I built a transparent computational bridge from a genome-scale CD4⁺ T-cell Perturb-seq atlas (Marson–Pritchard CRISPRi, 4 donors, conditions Rest / Stim 8 h / Stim 48 h) to tumor spatial transcriptomics (CosMx NSCLC, 765,771 cells, 960-gene panel) to ask a two-part question: within a single annotated CD4⁺ T-cell type, do spatially distinct functional states exist, and can the Perturb-seq atlas nominate a different candidate regulator for each — respecting that a knockdown's effect depends on whether the T cell is resting or activated.
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