Consistent with its p53‐independent tumor suppressive function, the levels of p73 targets including BAX, PUMA, and Caspase 3 are significantly increased in Pot1b∆/∆; p53−/− spleens Pot1b deficient telomeres induce p73 to activate BAX and PUMA, as the expression of both of these pro‐apoptotic genes is abrogated in p53−/−; p73−/− MEFs. Here, CASP3 is linked to neoplasm.