However, along with rapidly growing resistance to chemotherapy in patients with p53 abnormalities (both TP53 mutations and 17p deletion), and discovery of newer therapeutic options, CLB is often replaced by the purine analogs, such as fludarabine, monoclonal antibodies as rituximab, and other new agents involved in the apoptotic process or targeting pathogenic pathways of CLL cells, such as ibrutinib, venetoclax or chimeric antigen receptor T-cell therapy [1,2,3,4,16]. The gene discussed is CLYBL; the disease is B-cell chronic lymphocytic leukemia.