An inflammasome represents a high molecular weight complex that activates inflammatory caspases and activates cytokines of the IL-1 family (IL-1b, IL-18). Several inflammasomes have been described including the NLRP1 (NALP1) inflammasome, the NLRP3 (NALP3) inflammasome, the IPAF (NLRC4) inflammasome, the NLRP6 (NALP6) inflammasome, the RIG-I inflammasome and the AIM2 (absent in melanoma 2) inflammasome. Inflammasomes can be activated through multiple signals including live bacteria, microbial toxins, xeno-compounds, PAMPs and DAMPs. As IL-1β and other cytokines are key players in the inflammatory response, it is tempting to speculate that IL-1β, inflammatory caspases and inflammasomes play an important role in several diseases. Gout, an autoinflammatory disease characterized by severe joint inflammation, is associated with the deposition of MSU crystals in joints, among other characteristics. As MSU is a potent NLRP3 inflammasome agonist, it is believed that inflammasome-regulated IL-1β exerts a pathogenic role in gout. Furthermore, IL-1β secretion by the NLRP3 inflammasome is triggered by high extracellular glucose in β-cells. Elevated IL-1β is a risk factor for the development of Type 2 Diabetes Mellitus (T2DM) and contributes to insulin resistance. Thus by functioning as a sensor for metabolic stress, the NLRP3 inflammasome likely contributes to the pathogenesis of gout or T2DM, respectively.