Lipids, especially short-chain fatty acids, are a preferential source of acetyl groups for histone acetylation and epigenetic reprogramming.  FAO reprogram cellular metabolism and this oxidation is also the primary source of lipid-derived acetyl-CoA [62]. A recent finding shows that post-translational modifications such as acetylation, ubiquitination, and phosphorylation control FOXP3 expression, therefore, FAO supports the immunosuppressive function of Treg by regulating histone acetylation in the FOXP3 locus [63, 64] which stabilize the FOXP3 expression [65, 66] (Figure 1).