Various drugs targeting different pathways, such as PPAR agonists (elafibrinor and seladelpar), FGF analogs (aldafermin and pegbelfermin), apoptosis inhibitors (selonsertib and emricasan), and the CCR2/CCR5 inhibitor cenicriviroc, did not achieve the desired outcomes in terms of NASH resolution, fibrosis improvement, or hepatic fat reduction [96,97,98]. Here, CCR5 is linked to metabolic dysfunction-associated steatohepatitis.