Our findings that pan-HDAC inhibitor SFN increased Ace-H3K9 and Ace-H4K12 levels in the cerebral cortex of wild type mice and in SH-SY5Y cells, and countered the opposite effects by Aβ, provide clues about the mechanism of action of SFN with respect to AD pathology and behavioral symptoms. The gene discussed is HDAC9; the disease is Alzheimer disease.