With the former, SIRT3 plays critical role in increasing the deacetylation of Mn-SOD, which ultimately decreases the anion superoxide levels in mitochondria, whereas with the latter, SIRT3 plays a role in blocking NLRP3 inflammasome activation, which ultimately suppresses certain inflammatory responses involved in NASH pathogenesis [55]. The gene discussed is SOD2; the disease is metabolic dysfunction-associated steatohepatitis.