Thus, its inactivation is required for NAFLD development, confirmed by hyperlipidemia as well as fatty liver disease resulting from non-conservative inactivating mutations in the Wnt coreceptor LRP6 in mice and by the rescue of NAFLD using Wnt ligand Wnt3A [63,64,65]. This evidence concerns the gene WNT3A and metabolic dysfunction-associated steatotic liver disease.