The evidence that decreased Sirt4 expression in mice livers is able to protect against NAFLD by inhibiting MTPα deacetylation and degradation suggested that the upregulated levels of Sirt4 observed in NAFLD patients could contribute to the onset of the disorder by decreasing MTPα-catalyzed FAO and, consequently, by promoting ectopic lipid accumulation (12). This evidence concerns the gene HADHA and metabolic dysfunction-associated steatotic liver disease.