It is evident that in recent years, the idea of the complexity of cancer genetics has been gaining ground, wherein not only the presence and activity of genes carrying clearly pathogenic mutations (RAS, BRAF, p53, etc.)play a role, but also the additive effect (“dose effect”) of genes that, even if not being driver oncogenes, modify their activity in favor of dysregulating cancer‐related effects (proliferation, differentiation, production of growth factors, etc.). The gene discussed is TP53; the disease is cancer.