One model for the antitumor action of SAHA is that its inhibition of HDAC activity, and subsequent accumulation of acetylated histones, leads to the activation of genes whose expression causes induction of differentiation or apoptosis, thus inhibiting tumor growth, which is based on the finding that the expression of a relatively small number of genes (2–10 % of expressed genes) is regulated following exposure of tumor cells to vorinostat [61]. This evidence concerns the gene HDAC9 and neoplasm.