Progression of premalignant lesions into malignant tumors predominantly occurs through the loss of p53, INK4a and ARF35, whereas mechanisms enabling therapy-induced senescent cells to escape cell cycle arrest are highly context dependent and include the activation of CDK1/cdc236, maintenance of stem cells through ATR and/or Wnt-dependent37,38 pathways as well as activation of survival mechanisms39. This evidence concerns the gene CDKN2A and cancer.