These results can be explained by the fact that SFRP5 is an anti-inflammatory molecule that seems to have a protective role in the first steps of hepatic steatosis, but then the inflammation seems to deregulated SFRP5 signaling, blocking its inhibition of the noncanonical WNT pathway, which promotes NAFLD progression. The gene discussed is SFRP5; the disease is metabolic dysfunction-associated steatotic liver disease.