This indicates that secondary oncogenic alterations are required for TP53/RB1-deficient neuroendocrine cells in the lung epithelium to become malignant, an idea which has been validated by the generation of SCLC GEMMs that, in addition to the Cre-mediated deletion of TP53 and RB1, also harbor further genetic aberrations and demonstrate a shorter tumor latent period [21,22,23,24,25,26,27,28]. Here, TP53 is linked to neoplasm.