CDKN2A and neoplasm: We used cisplatin and doxorubicin to challenge two melanoma cell lines, the B16F10 cells that were derived from a spontaneously generated mouse melanoma tumor [8] and the recently established YUMM1.7 (Yale University Mouse Melanoma) cell line engineered to recapitulate three human‐relevant melanoma driver mutations [9]; the BrafV600E mutation that activates proliferative signaling and two tumor suppressor loss‐of‐function mutations Pten−/− and Cdkn2a−/− [9, 10, 11, 12].