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Use when building server-driven UIs with htmx, designing hx-* attribute compositions, choosing swap strategies (innerHTML/outerHTML/morph), wiring out-of-band updates, integrating with form validation, or migrating from a SPA back to server-rendered HTML. Triggers: hx-get/hx-post setup, hx-target + hx-swap interplay, hx-trigger debouncing, OOB swaps for parts of the page outside the request target, response headers like HX-Trigger and HX-Push-Url, integration with Hyperscript or Alpine.js, accessibility considerations on partial updates. NOT for full SPAs (use React/Vue), framework-specific server libraries (use those skills directly), or non-HTML responses.

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Target a specific Google Chrome user profile for browser automation via CDP. Discovers installed profiles from the Chrome Local State file, launches Chrome with the requested profile attached to a debug port, and connects agent-browser via `agent-browser connect <port>`. Use when "automate using my Work/Personal Chrome", "open site with my saved session", or "use Chrome profile named <name>". NOT for headless scraping without an existing user profile (use mk:agent-browser directly); NOT for importing cookies only (use agent-browser --auto-connect state save).

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Arm proactive 5-hour usage protection for long Claude Code sessions (batch, subagents, high window % at start). Daemon reads account-level 5-hour window usage (not per-session). User types /usage-guard at session start. Re-arm every sitting. If user mentions usage-guard by name, read this file and run arm.sh.

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Generalize published Spectre and remote microarchitectural research into passive target prerequisites, defensive review, and approval-gated local validation. Use for shared runtimes, JavaScript isolates, edge workers, serverless platforms, browser sandboxes, remote timing, cache side channels, speculative type confusion, or Dynamic Process Isolation analysis.

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Use when a network probe, DNS lookup, HTTP fetch, or nmap scan reports the target host or the internet is unreachable. Stops further probing and reports a target-readiness blocker with useful diagnostics.

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Safely develop, verify, and document proof-of-concept exploits and payloads for authorized targets inside isolated Workspace Containers. Use when a Hypothesis is well-founded, target authorization covers scope, and each active step will carry a durable approval — for minimal PoCs, impact verification, or reproducible exploit Evidence.

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Estimates the minimum biological replicates (or cells/events) for a target power at a target FDR in genomics experiments using ssizeRNA, PROPER, powsimR for scRNA-seq, and pilot-data dispersion estimation from DESeq2/edgeR. Covers the biological-versus-technical replication distinction (technical replicates do not add degrees of freedom for biological inference), replicate-number-versus-sequencing-depth budgeting, scRNA-seq sample-versus-cell allocation under a pseudobulk model, and the critique that "n=3" is a publication convention rather than a power calculation. Use when budgeting a sequencing experiment, writing the sample-size justification in a grant, estimating replicates from pilot data, allocating a fixed budget between samples and depth, or planning scRNA-seq cohort size. For clinical-trial sample size see clinical-biostatistics/power-and-sample-size; for the power-given-n direction see experimental-design/power-analysis.

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Visualises RNA-modification data with transcript-feature metagene plots (Guitar GuitarPlot; MetaPlotR; deepTools computeMatrix scale-regions), peak-centred heatmaps (ComplexHeatmap; deepTools plotHeatmap), IP-vs-input paired browser tracks (log2 IP/input bigWig via deepTools bamCompare; pyGenomeTracks; Gviz; IGV/UCSC track hubs), DRACH sequence-logo plots (ggseqlogo; MEME), feature-distribution stacked bars, and volcano/MA plots for differential modification. Establishes stop-codon enrichment in the metagene plot as the biological QC anchor for any MeRIP dataset (Dominissini 2012; Meyer 2012). Use when producing the canonical metagene plot with stop-codon enrichment as a QC anchor, building paired IP/input genome-browser tracks at single-locus resolution, plotting peak-centred heatmaps clustered by condition, summarising peak distribution across transcript features, generating DRACH motif logos as sanity checks, rendering volcano plots of differential m6A, or reproducing the stop-codon enrichment plot.

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Designs pooled sgRNA libraries for CRISPR knockout, interference (CRISPRi), activation (CRISPRa), Cas12a multiplex, base-editor, and prime-editor screens. Covers on-target scoring (Rule Set 2, Azimuth, DeepSpCas9, CRISPRon), off-target scoring (CFD, MIT), TSS-relative positioning for CRISPRi/a (Horlbeck, Dolcetto, Calabrese), PAM-variant chemistries, control-guide composition, oligo cloning architecture, and library QC. Use when choosing a genome-wide library (GeCKOv2 vs Avana vs Brunello vs TKOv3 vs Inzolia), designing a focused or paralog-focused custom library, picking CRISPRi vs CRISPRa TSS windows, deciding control-guide proportions, or diagnosing library skew and dropout in a freshly cloned pool.

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Designs and analyzes in vivo CRISPR screens in animal tumor models, organoids, and immune-cell adoptive transfers. Covers bottleneck math (250x cells/sgRNA requires ~25M cells implanted; impossible for most syngeneic models, forcing focused libraries), focused library design (Manguso 2017 Nature 547:413 immune screen; Chen 2015 tumor screens), CRISPR-StAR intrinsic-control screening (Uijttewaal 2025 Nat Biotechnol 43:1848), clonal-dynamics-limited detection, tumor-explant DNA recovery, syngeneic vs xenograft vs PDX considerations, and the relationship to downstream MAGeCK / drugZ analysis. Use when designing in vivo CRISPR screens for tumor / immune / metastasis biology, choosing focused vs genome-wide for animal models, addressing bottleneck-induced clonal collapse, picking the syngeneic / xenograft / PDX model, integrating in vivo with in vitro results, or applying CRISPR-StAR for animal experiments.

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Quantifies CRISPR editing outcomes with CRISPResso2 (Clement 2019 Nat Biotechnol) across Cas9-nuclease (indels, HDR), CBE and ABE base editors (target conversion + bystander), and prime editor (pegRNA-templated) modes. Covers single-amplicon (CRISPResso), multi-sample batch (CRISPRessoBatch), pooled-amplicon (CRISPRessoPooled), WGS off-target (CRISPRessoWGS), and sample-comparison (CRISPRessoCompare) workflows; quantification-window math that controls what is called edited; substitution-vs-indel diagnostic to distinguish BE from Cas9 contamination; MMEJ deletion pattern interpretation; allele-frequency tables; and failure modes from amplicon misalignment or contamination. Use when quantifying editing from amplicon sequencing, choosing CRISPResso mode by design, distinguishing intended edits from bystanders and indel byproducts, debugging low-alignment runs, or generating publication-grade editing reports.

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Designs covalent inhibitors and warheads targeting cysteine, lysine, serine, threonine, tyrosine, and aspartate residues, with explicit handling of warhead reactivity (acrylamide, chloroacetamide, vinyl sulfone, sulfonyl fluoride, fluorosulfate, aldehyde, boronate, nitrile), reversibility (kinact/Ki, t_residence), glutathione (GSH) stability, intrinsic reactivity assays, and covalent docking (DOCKovalent, GOLD, HCovDock). Use when designing covalent inhibitors for targeted covalent inhibition (TCI), KRAS G12C-style approaches, or rationalizing covalent SAR.

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Align preprocessed CLIP-seq reads (eCLIP, iCLIP, iCLIP2, PAR-CLIP) to genome with STAR or bowtie2 using crosslink-preserving parameters, choosing between unique-mapper-only and multi-mapper-aware alignment for repeat-binding RBPs, deciding STAR vs HISAT2 memory trade-offs, and applying ENCODE-compatible filters. Use when turning preprocessed CLIP FASTQ into a deduplicated, MAPQ-filtered BAM ready for peak calling or crosslink-site detection.

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Identifies essential genes from CRISPR-Cas9 fitness screens using BAGEL2 (Kim & Hart 2021 Genome Med), a Bayesian classifier scoring per-gene Bayes Factors via log-likelihood ratios over per-sgRNA fold changes, calibrated against CEGv2 core-essentials (Hart 2017 G3, ~684 genes) and NEGv1 non-essentials (Hart 2014, ~927 genes). Covers the fc + bf + pr workflow, the linear-extrapolation improvement over BAGEL1 truncation, multi-target off-target correction, tumor-suppressor sensitivity (BAGEL2 detects enrichment), and BF calibration (BF >6 ≈ 90% posterior per Hart 2017; ~5% FDR by BAGEL convention). Use when classifying essential vs non-essential genes, calibrating BAGEL2 thresholds against PR curves, identifying tumor suppressors alongside essentials, comparing BAGEL2 hits to MAGeCK / drugZ, or generating publication-quality essentiality calls.

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Queries PharmGKB / CPIC / DPWG for drug-gene interactions; calls CYP2D6/CYP2C9/CYP2C19/DPYD/TPMT/NUDT15/UGT1A1/SLCO1B1 star alleles and phenotype with PharmCAT, Cyrius (CYP2D6 structural variants), Aldy, Stargazer; applies Caudle 2020 activity-score translation. Use when implementing pharmacogenomic-guided prescribing, applying CPIC vs DPWG guidance, screening HLA risk alleles for ICI / antiepileptics / abacavir, or interpreting compound TPMT+NUDT15 thiopurine risk.

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Predict enhancer-gene regulatory connections from ATAC-seq using ABC, ENCODE-rE2G, HiChIP, or Cicero. Use when linking distal enhancers to target genes, choosing between contact-aware (ABC, ENCODE-rE2G), accessibility-only (Cicero), and orthogonal (HiChIP H3K27ac, EpiMap) approaches, validating predictions against CRISPRi-FlowFISH gold-standard, or building cell-type-specific regulatory maps for fine-mapping or therapeutic target discovery.

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Query BindingDB for measured drug-target binding affinities (Ki, Kd, IC50, EC50). Search by target (UniProt ID), compound (SMILES/name), or pathogen. Essential for drug discovery, lead optimization, polypharmacology analysis, and structure-activity relationship (SAR) studies.

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Determines if current hormone levels are within target range for affirmed gender (e.g., testosterone 400-700 ng/dL for transgender males, estradiol 100-200 pg/mL for transgender females). Triggers include patient on hormone therapy and time for level check.

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Recommends real-time continuous glucose monitoring (RT-CGM) for adult patients with type 1 diabetes mellitus (T1DM) whose hemoglobin A1C is above individualized target. Consider when clinician notes 'T1DM A1C above goal, consider RT-CGM' or 'Patient willing to wear CGM daily, A1C elevated'.

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This skill recommends obtaining serum free T4 and prolactin levels within 1–2 weeks after transsphenoidal surgery (TSS) for Cushing's syndrome to screen for overt hypopituitarism. Use in postoperative Cushing's syndrome patients during the early recovery window when evaluating for new pituitary hormone deficiencies.

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Suggests repeat transsphenoidal surgery for patients with persistent hypercortisolism after initial transsphenoidal surgery when imaging shows evidence of incomplete resection or a pituitary lesion. Clinical triggers include postoperative MRI revealing residual adenoma, persistent elevated UFC or late-night salivary cortisol, and visible pituitary lesion on imaging.

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This skill suggests pituitary-directed medical treatments (e.g., cabergoline, pasireotide) for patients with Cushing's disease who are not surgical candidates or have persistent disease after transsphenoidal surgery. Use when a CD patient cannot undergo surgery or has residual disease post-TSS; triggers include "not a surgical candidate", "persistent disease after TSS", "ongoing hypercortisolism despite prior surgery".

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This skill suggests targeted therapies (somatostatin analogs or tyrosine kinase inhibitors) to treat ectopic ACTH syndrome when ectopic ACTH secretion is confirmed or strongly suspected. Use when triggers include occult or metastatic ectopic ACTH secretion, very severe ACTH‑dependent disease uncontrolled by medical therapy, or when surgery is not possible or noncurative.

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This skill recommends localizing and resecting ectopic ACTH-secreting tumors with node dissection when ectopic ACTH secretion is suspected or confirmed. Clinical triggers include unexplained persistent hypercortisolism after pituitary surgery, elevated ACTH with negative pituitary MRI, or identification of occult ectopic ACTH syndrome (EAS) on biochemical testing.

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