As in the case of most tumor suppressors, the indirect interplay of p53 with CMYC, KRAS or telomerase also includes a passive LOF contribution—when mutated or otherwise inactivated WT TP53, which normally may inhibit the oncogenes, loses this function and thus allows the oncogenes to promote neoplastic phenotypes [49,50,51]. This evidence concerns the gene TP53 and neoplasm.