Thus, the former oncogenes, such as Ras, Myc, etc. cause endogenous DNA damage at early stages of tumorigenesis, triggering cell cycle checkpoints and the ensuing cellular senescence or cell death, events that originally led us and others to formulate the concept of DDR as an intrinsic barrier against activated oncogenes and tumor progression of major types of carcinomas [53–55]. The gene discussed is MYC; the disease is neoplasm.