Thus, our results of positive association of elevated serum ALT and the Met196Arg variant in TNFRSF1B with SUA concentrations among subjects with NAFLD further support this proposal, which is called damage associated molecular patterns (DAMPs), and suggested that the release of UA might be accelerated when tissue injury (combined with a genetic susceptibility to inflammation) happened in NAFLD patients [41]. This evidence concerns the gene TNFRSF1B and metabolic dysfunction-associated steatotic liver disease.