A potential mechanism for the combination of the BET inhibitor ABBV-075 and the BCL2 inhibitor venetoclax (NCT02391480) in patients with AML is that venetoclax monotherapy increases MCL1 protein levels, whereas combination therapy with ABBV-075 results in a reduction in both MCL1 and Bcl-xL levels and together induces tumor cell apoptosis.173,174. The gene discussed is DNER; the disease is acute myeloid leukemia.