The level of tumor MHC-I expression in fresh biopsies reflects T-cell activity and consequently IFNγ production, as demonstrated by (i) loss of MHC-I expression in IFNγ-resistant cells [77], (ii) identification of IFNγ signaling pathway components as essential mediators of tumor sensitivity to immune-mediated killing, in global genome-scale screens [202,203,204] and (iii) an increase in longitudinal IFNγ gene signatures early during therapy with immune checkpoint inhibitors in responding melanoma patients [75,212]. The gene discussed is IFNG; the disease is melanoma.