Given the near-universal occurrence of TP53 gene mutations in human SCLC and the obligatory requirement for TP53 gene inactivation in the pathogenesis of murine SCLC [61], we proposed a concept to exploit the differential biology of inactivating versus gain-of-function TP53 mutations to tailor therapy in SCLC. This evidence concerns the gene TP53 and small cell lung carcinoma.