We demonstrate that p16 suppression in the lung epithelium in vivo is a unique RB1 function, differing from the shared p107 and p130 function in fibroblasts.15 We also show that unlike in murine and human fibroblasts, RB1 loss in lung epithelial progenitor cells is sufficient to enhance growth providing evidence that p16/RB1 pathway function is distinct in epithelial cells.20, 21, 22 Importantly, p16 induction after RB1 loss was not associated with cellular senescence but rather protected lung epithelial progenitor cells from DNA damage and development of aggressive lung cancers. The gene discussed is RB1; the disease is lung cancer.