The relevance of these findings to NASH is that systemic adiponectin levels progressively diminish in human steatosis and NASH [55,56,57,58], while AdipoR2 exhibits suppressed expression in human NASH livers and in human hepatocytes from NASH patients [53,59,60,61]: a collectively diminished adiponectin axis in the liver may account for increased CCN2 (and TGF-β) in non-fibrotic NASH. This evidence concerns the gene ADIPOR2 and metabolic dysfunction-associated steatohepatitis.