Given that p53 mutations occur in 50% of all human cancers 22, 23, 24 and in a high proportion of triple‐negative breast cancer (TNBC) cells 25, we next wanted to extend these studies to investigate whether caspase‐2 activation and SK1 proteolysis are deregulated in these situations and if so, whether SK1 proteolysis can be restored by activation of the CHK1‐suppressed pathway in p53‐mutant TNBC cells. The gene discussed is CHEK1; the disease is cancer.