In particular, NASH, but not simple steatosis, is associated with the regulation of genes in the liver which are associated with atherosclerotic risk and, as such, may contribute to the pro-atherogenic state [5]: circulating levels of several inflammatory markers (C-reactive protein, interleukin-6, monocyte chemotactic protein 1, and TNF-α), procoagulant factors (plasminogen activator inhibitor 1, fibrinogen, and factor VII), and oxidative stress markers are highest in patients with NASH, intermediate in those with simple steatosis, and lowest in control subjects without steatosis [92,93]. This evidence concerns the gene CCL2 and steatosis.