Our findings revealed that Sin A treatment significantly inhibited the mRNA levels of hepatic genes, previously functionally linked to lipid synthesis, especially, Srebp1c, Acaca, Fasn, Mogat1, and Pparg. Considering that inflammation response is highly linked with the progression from NAFLD to NASH, we examined the mRNA levels of hepatic inflammatory mediators, previously functionally linked to inflammation response. Here, ACACA is linked to metabolic dysfunction-associated steatohepatitis.