cSCC, UV-driven and highly mutagenic, is immunogenic yet exploits adaptive resistance: IFN-γ–induced PD-L1 upregulation on tumor and myeloid cells attenuates antitumor T-cell activity, reinforced by Tregs, IL-10/TGF-β, M2 macrophages, and impaired type I IFN signaling [90,91,92,93]. Here, TGFB1 is linked to neoplasm.