As neither whole-body Cmklr1 deficiency and hematopoietic deletion of Cmklr1 in Ldlr-/- mice affected the development of NAFLD, the alterations in chemerin and Cmklr1 levels found in humans and mouse models of NAFLD may be a secondary effect of the metabolic syndrome and NAFLD [10]–[12], [14]. This evidence concerns the gene RARRES2 and metabolic dysfunction-associated steatotic liver disease.