Thus, its inactivation is necessary for NAFLD development, as evidenced by dyslipidemia and fatty liver disease in mice carrying non-conservative inactivating mutations in the Wnt coreceptor LRP6, and the rescue of NAFLD by Wnt ligand Wnt3a (Go et al., 2014). This evidence concerns the gene WNT3A and metabolic dysfunction-associated steatotic liver disease.