Indeed, choline-deficient amino acid-defined diet-induced steatosis, inflammatory cell infiltration, and liver fibrosis with increased hepatic expression of CCR2 and CCL2, while the KC depletion improved NASH with a decrease of CCL2 expression and recruitment of Ly6C− monocytes that exhibit a typical M2 anti-inflammatory phenotype [126]. Here, CCL2 is linked to metabolic dysfunction-associated steatohepatitis.