Since AKT was also shown to directly phosphorylate other histone modifiers, such as the H3K9/H3K27 methyl transferase EZH2 [131], it is conceivable that the frequent dysregulation of the PI3K/AKT pathway observed in cancer cells leads to more global changes in epigenetic regulation of splicing programs through altered genome-wide recruitment of RBPs. Here, AKT1 is linked to cancer.