H2BC12L and acute myeloid leukemia: Fiskus et al. reported that by inducing hyperacetylation of lysine residues on histone proteins, panobinostat could induce greater dependency on the BRD4-regulated transcription of oncoproteins in acute myelogenous leukemia (AML) such that cotreatment with panobinostat and JQ1 synergistically leads to growth inhibition and apoptosis in cultured and primary AML cells [16].