In the present study, we performed a molecular docking analysis and found that SIRT6, as the ATL I targeted effector, increased deacetylation activity to activate PPARα and also increased its target genes to accelerate fatty acid oxidation, accompanied by attenuating NFκB-mediated NLRP3 inflammasome formation to inhibit hepatic lipid accumulation-induced hepatic inflammation and steatosis (Figure 8). This evidence concerns the gene NLRP3 and steatosis.