Obviously, if this holds true, such a mechanism would assign a yet ambiguous context to LD biogenesis in NAFLD/NASH (as well as alcoholic AFLD): slowing disease progression in a paracrine mode via the CCN1-mediated deceleration of inflammation-associated fibrosis at the cost of promoting steatosis progression via an autocrine amplification loop. This evidence concerns the gene CCN1 and metabolic dysfunction-associated steatohepatitis.