Indeed the loss of p130 in Rb-deficient cells promotes the development of neuroendocrine lesions in the lungs of mice [10], deletion of Rb and p130 in lung epithelial cells leads to hypercellularity due to defective apoptosis [8]; and p130 acts as a tumor suppressor in the context of Rb and p53 loss (rendering SCLC [9] or NSCLC [30] depending on the targeted cell compartment) or Kras activation (rendering NSCLC [39]). This evidence concerns the gene KRAS and non-small cell lung carcinoma.