While the paucity of mutations may support the notion of an inherent capacity of mouse SCLC to metastasize, the nearly intact cell-matrix and cell-cell interactions seen in Rb1/Trp53-deficient preneoplastic cells (hereafter called preSCs), derived from early-stage lesions in GEMMs, imply the need for additional drivers to induce drastic cellular transformation72,73. The gene discussed is TP53; the disease is small cell lung carcinoma.