We also examined the histone acetylation mark H4K16ac and discovered a decrease in the brains of AD patients [9], and studies in fly models of AD suggest a protective role of H4K16ac against AD pathology-related insults [68, 69] Additionally, in a mouse model of AD, the histone deacetylase HDAC2 increases and H4K12ac decreases [70], and an ameliorative effect was demonstrated in an AD mouse model of increasing acetyl-CoA synthetase 2 (ACSS2) [71], which generates acetyl-coA and regulates histone acetylation in rodent hippocampus to promote memory [72, 73]. The gene discussed is ACSS2; the disease is Alzheimer disease.