In recent years, novel agents targeting critical processes and pathways such as microenvironmental interactions (e.g. BTK inhibitors) and apoptotic cell death (e.g. BCL-2 inhibitors) have revolutionized the management of chronic lymphocytic leukemia (CLL), leading to high overall response rates (often exceeding 90%) and superior progression-free and, at least in some trials, overall survival compared to classic chemoimmunotherapy (1). The gene discussed is BCL2; the disease is B-cell chronic lymphocytic leukemia.