Inhibition of CCL2/CCR2 or CCL5/CCR5 has been shown to attenuate liver fibrosis in mice [41,42,43], and a recent phase 2b clinical trial showed that treatment with the CCR2/5 antagonist cenicriviroc resulted in an early antifibrotic benefit that was maintained particularly in the subset of NASH patients with advanced fibrosis [44]. This evidence concerns the gene CCL5 and metabolic dysfunction-associated steatohepatitis.