The emergence of an array of highly effective targeted therapies that exploit several intrinsic vulnerabilities of chronic lymphocytic leukemia (CLL) cells, particularly small molecules that target Bruton’s tyrosine kinase (BTK) to interfere with B-cell receptor (BCR) signaling or the anti-apoptotic function of B-cell lymphoma (BCL-2), has transformed the treatment landscape of this disease and made it one of the most gratifying hematologic malignancies to treat. The gene discussed is BCL2; the disease is B-cell chronic lymphocytic leukemia.