As guided by knowledge-based algorithms, we hypothesized that (1) circulating CCL-2 levels should be elevated in patients with NAFLD due to an increase in its secretion from enlarged visceral adipose tissue and as evident by monocyte infiltration into the NAFLD livers; and (2) deregulated insulin signaling in adipose tissue increases Fas/FasL expression and its release into the bloodstream that promote an apoptosis of hepatocytes. Here, CCL2 is linked to metabolic dysfunction-associated steatotic liver disease.