Interestingly, pharmacological inhibition of SIRT2 blocks the therapeutic action of NAD+ against NAFLD pathologies [17], while SIRT2 deficiency reprograms T-cell metabolism by targeting metabolic enzyme hyperacetylation, leading to a more effective antitumor immune response in the tumor microenvironment [18]. The gene discussed is SIRT2; the disease is metabolic dysfunction-associated steatotic liver disease.