These data suggest that in EGFR/TP53 co-mutated NSCLC, apCAFs (Fib_CD74+) regulate CD8+ T cell function by recruiting Tregs, amplifying the immunosuppressive chemokine network, and remodeling the extracellular matrix, thereby cooperating with tumor cells to drive cytotoxic CD8+ T cells from an activated state toward exhaustion. The gene discussed is CD8A; the disease is neoplasm.