Moreover, IFNγR1KO melanoma was completely resistant to anti-CTLA-4, consistent with the reduced sensitivity of IFNγR1KD melanoma to anti-CTLA-4 treatment.9 Using this “clean” model, our first interesting finding was that unlike IFNγR1KD melanomas that had largely normal TILs,9 IFNγR1KO melanomas had much reduced abundance of CD8+ TILs at the baseline and did not show increased infiltration and functional rejuvenation of TILs upon anti-CTLA-4, establishing an active role of melanoma IFN-γ in shaping TILs. This evidence concerns the gene CTLA4 and melanoma.