Bcl-2; bortezomib; multiple myeloma; t(11;14); venetoclax

Multiple myeloma (MM) is the second most common blood cancer caused by the uncontrolled proliferation of clonal plasma cells. Despite recent advances in treatment, a majority of patients eventually relapse and die because of progressive disease (PD). Thus, the development of modern molecules with novel mechanisms of action is needed. The overexpression of antiapoptotic proteins (ie, Bcl‐2, Bcl‐XL, Mcl‐1) represents one of the hallmarks of cancer that favors tumor cell survival. It has been demonstrated that a subset of MM is Bcl‐2 dependent. These are especially those harboring the t(11;14)—molecular subgroup which is associated with a high expression of Bcl‐2 and a low expression of Bcl‐XL and Mcl‐1.1, 2 The presence of translocation t(11;14) is present in 15%‐20% of newly diagnosed MM3 and even up in 50% of primary plasma cell leukemia.4