Taken together, our mechanistic dissection of three important tumor suppressor genes of KRAS-driven carcinogenesis provides strong in vivo genetic evidence that SNAIL bypasses senescence and drives tumour development independent of TRP53 inactivation and downstream of the p16Ink4a cell cycle restriction check-point, e.g., via blocking the RB-controlled senescence-pathway. Here, KRAS is linked to neoplasm.