Targeting ACER3 could alleviate the severity of NASH by suppressing the hepatocellular oxidative stress, thus attenuating early inflammation and fibrosis but not steatosis, demonstrated by the similar area of steatosis and significantly reduced number of inflammatory foci, lower expression levels of IL-6, TNF-α and TGF-β, and minor fibrosis in Acer3−/− mice (146). Here, IL6 is linked to metabolic dysfunction-associated steatohepatitis.