Due to this, these drugs may also be less likely to exert the same selective pressure as chemotherapy drugs, which were described to boost the frequency of pre-existing clones harboring pro-cancerous mutations in tumor suppressor genes such as TP53. The observation that sublethal necroptotic signaling was non-mutagenic provides hope that drugs which destroy cancer cells via necroptosis may be less prone to trigger development of second cancers than chemotherapy or radiotherapy, or possibly even than direct apoptosis inducers. This evidence concerns the gene TP53 and cancer.