We show that melanoma cell-derived Activin-A indirectly inhibits CTL accumulation and proliferation, likely by interfering with the CXCL9/10-CXCR3 chemokine axis, and that its expression correlates with resistance to anti-PD1 therapy in melanoma patients and impairs the response to an anti-PD1/anti-CTLA4 combination in BRAF-driven mouse melanoma. The gene discussed is PDCD1; the disease is melanoma.