In melanoma, subclones with deleterious mutations in the interferon (IFN)-γ pathway are paradoxically well controlled by the immune system due to the downregulated tumor expression of programmed death ligand 1 (PD-L1), but these cells exhibit immune resistance when supplementary PD-L1 signaling is provided by nearby IFN-γ-intact subclones [30]. The gene discussed is IFNG; the disease is melanoma.