A recent study showed that SIRT2-mediated deacetylation of NLRP3 ameliorates NLRP3 inflammasome activation, thus contributing to protection against aging-associated inflammation and insulin resistance.69 However, it is unclear whether multiple Lys residues of NLRP3 are acetylated or deacetylated under basal conditions and which upstream signals regulate the acetylation of NLRP3 at certain phases of inflammasome activation. The gene discussed is NLRP3; the disease is Insulin resistance.