Li et al. (2023) discovered that it could protect against hepatic steatosis. Furthermore, SIRT2-deficient mice were more susceptible to obesity caused by a high-fat, high-cholesterol, and high-sucrose diet, which exacerbated steatohepatitis. In addition, SIRT2 has been demonstrated to inhibit the activity of NLRP3 inflammatory vesicles and modulate the acetylation of p65, thereby playing a regulatory function in inflammatory processes (Liu et al., 2021; Yan and Horng, 2020). However, its role in FAO, especially CPT1A, remains underexplored. This evidence concerns the gene SIRT2 and fatty liver disease.