Conventionally, p53 is reported to suppress tumors through cell-autonomous functions, representatively inducing cell apoptosis through transactivating pro-apoptotic targets and inducing cell-cycle arrest (also cell senescence) through transactivating targets such as CDKN1A. Indeed, we previously reported that ATO could effectively suppress tumor xenografts in various immunodeficient mouse models.18 The gene discussed is CDKN1A; the disease is neoplasm.