In contrast with these studies, we observed no effects on erythroid development upon treatment with VPA, suggesting that the remaining levels of HDAC1 (and HDAC2) are sufficient for erythroid development, or that VPA treatment results in increased activity of other HDAC, including HDAC9, which has been demonstrated in AML cells, and has been functionally linked to erythroid development, as well as the pathogenesis of myeloproliferative disorders [64, 65]. This evidence concerns the gene HDAC1 and acute myeloid leukemia.