In murine skin, targeted activation of the RAS/RAF/mitogen-activated protein kinase (MAPK) pathway, coupled with deletion of Tgfbr1 in LGR5+ve stem cells, promotes rapid development of cSCC, which, in the absence of wounding, may mimic the kinetics of tumour induction in vemurafenib-induced cSCC. The gene discussed is LGR5; the disease is neoplasm.