Although the precise function of TM6SF2 in the context of NAFLD is mostly unknown, a study by Li et al. demonstrated that overexpression of TM6SF2 reduced hepatic lipid accumulation in HFD-fed mouse models, whereas knockdown of TM6SF2 was shown to promote inflammation and hepatic lipid accumulation [12]. This evidence concerns the gene TM6SF2 and metabolic dysfunction-associated steatotic liver disease.