Deacetylation of PPARγ at K268 and K293 (Figure 2c,d) can set off a series of reactions, ranging from recruiting brown adipose tissue program coactivators, promoting white fat browning to increasing thermogenesis, exhibiting increased energy expenditure, significantly suppressing obesity and improving insulin sensitivity (same as TZDs), to reducing fat accumulation, bone loss, edema, and congestive heart failure [42]. This evidence concerns the gene INS and obesity disorder.