These pathologically distinct conditions converge on a similarly dysregulated microenvironment characterized by interconnected processes such as aberrant TGF-β signaling that drives stromal activation and ECM remodeling; PD-L1-mediated immune evasion that attenuates antitumor immunity and promotes disease progression;10,11 and progressive ECM stiffening that potentiates both fibrotic advancement and tumor invasion.12,13. The gene discussed is TGFB1; the disease is neoplasm.