Since HDAC2 and HDAC4 catalyse the deacetylation of lysine residues on histones H2A, H2B, H3, and H4, and KDM1A catalyses demethylation at H3K4me and H3K9me, we hypothesised that the differential phosphorylation of these epigenetic modifiers, following RTK inhibition, may account for the decrease in H3K4me3 and H3K27ac at the PHLDA1 locus observed in our breast and endometrial cancer models. The gene discussed is HDAC2; the disease is endometrial cancer.