Vandanmagsar et al. also showed that NLRP3 could identify uric acid, ATP, fatty acids, and other endogenous signals; in addition, it might be activated by a lysosome-dependent pathway, which resulted in increased expression of IL-1β and other proinflammatory cytokines in the macrophages and induced insulin resistance in the adipose tissues, muscles, liver, and other peripheral tissues [35]. The gene discussed is IL1B; the disease is Insulin resistance.