Thus, it is possible that over the course of this study, overexpression of Hdac9 could have led to β cell dysfunction/depletion and reduced insulin secretion, which in turn could have contributed to the adverse metabolic phenotype (i.e., adipocyte hypertrophy, hepatic steatosis) observed in the aged HDAC9 TG mice. This evidence concerns the gene HDAC9 and Hepatic steatosis.