The oncogenic stress induced by these DNA-damaging agents stimulates various aspects of anti-cancer immunity, including activation of NK cells via ULBP1, MICA/B, and PVR expression at the surface of the cancer cell in an ATM (ataxia telangiectasia, mutated), ATR (ATM- and Rad3-related) protein kinases, and/or P53-dependent manner (8, 96–99). The gene discussed is ATM; the disease is cancer.