Tumor survival is further supported by widespread TP53 mutations (seen in most HGSC) disrupting p53-dependent apoptosis [6], alongside with B-cell CLL/lymphoma 2 (Bcl-2) overexpression, TCTP–p53/myeloid leukemia-1 (Mcl-1) interactions, and impaired caspase activity [7]. The gene discussed is TP53; the disease is B-cell chronic lymphocytic leukemia.