Indeed, inactivating mutations in tumor suppressor genes (such as TP53) and retinoblastoma transcriptional corepressor 1 (RB1) or activating alterations in oncogenes (e.g., Kirsten rat sarcoma virus (KRAS), myelocytomatosis oncogene (MYC)) are key events in tumor initiation [57,63,64]. The gene discussed is TP53; the disease is neoplasm.