Conversely, in other fusion-protein driven leukemias, binding sites of AML::ETO and PML::RARα are characterized by low H2A.Z acetylation.58 One study suggested that H2A.Z could have a higher affinity for atypical retinoids, thus linking DNA damage with histone variants in PML::RARα-positive leukemia cells.57 In the context of a lymphoid cancer, a reduction of H2A.Z levels and its extensive genomic redistribution accompanied Myc-driven B-cell transformation.59 This evidence concerns the gene RUNX1T1 and acute myeloid leukemia.