Additionally, since similar to other BETis, ABBV-075 treatment attenuated MYC and CDK6, while simultaneously inducing HEXIM1 and CDKN1A (p21)11,12,44–47; these perturbations also likely augmented venetoclax-mediated inhibition of growth and survival of AML BPCs. The gene discussed is HEXIM1; the disease is acute myeloid leukemia.