Several clinical studies have upheld a role for a low circulating adiponectin level in the pathogenesis of NAFLD and confirmed the strong association among reduced adiponectin production by adipose tissue, NAFLD, and IR, together with the hypothesis that an imbalance between pro-inflammatory and anti-inflammatory cytokines may have a pathogenic role in the development of liver damage in NAFLD [58]. This evidence concerns the gene ADIPOQ and metabolic dysfunction-associated steatotic liver disease.