The NLRP3 inflammasome can be hyperactivated by a wide variety of DAMPs [26] (i.e., glucose, extracellular ATP, gout-linked etiologic agents such as calcium pyrophosphate dehydrate crystals and uric acid crystals, dietary saturated fatty acids, etc.)[27], resulting in the direct release of pro-inflammatory inflammasome-related ILs, e.g., 1β and 18 [26]. The gene discussed is NLRP3; the disease is gout.