In contrast to other AML subsets, VPA inhibits not only the mature AML cells but also the immature progenitors in AML1/ETO [17]. The drug targets the AML1/ETO-HDAC complex, and thereby alters gene expression and induces differentiation [31]. VPA has specific effects in this AML subset. The drug induces differentiation followed by apoptosis and accompanied by increased expression of repressed AML1 target genes [31]. Here, HDAC9 is linked to acute myeloid leukemia.