The potential of targeting BAP1 in myeloid malignancies with ASXL1 mutations (Fig. 5) was demonstrated by Wang et al. who corroborated that truncated ASXL1 stabilized BAP1 and increased its recruitment to leukemogenic gene loci for their activation and then used a biochemical screen to identify a BAP1 catalytic inhibitor that delayed disease progression in NSGS mice engrafted with leukemic cells from a patient diagnosed with de novo AML harboring an ASXL1 truncation mutation (p.Q588*) [102]. The gene discussed is BAP1; the disease is acute myeloid leukemia.