In the setting of non-alcoholic fatty liver disease (NAFLD)/non-alcoholic steatohepatitis (NASH), it was initially reported that RIPK3 might maintain white adipose tissue homeostasis and prevent glucose intolerance by regulating caspase-8 expression, thus reducing adipose tissue apoptosis and inflammation [2,57,59,69,70,71]. This evidence concerns the gene RIPK3 and metabolic dysfunction-associated steatohepatitis.