Although the exact mechanisms of how pathogenic particles drive inflammation is not completely understood, it has been shown that danger-associated molecular patterns, such as endogenous uric acid (gout) or cholesterol (atherosclerosis) as well as exogenous particles like asbestos (asbestosis) or crystalline silica (silicosis), share features of crystalline particles that activate the NLRP3 inflammasome (also known as CIAS1, NALP3, or cryopyrin) (18–20). The gene discussed is NLRP3; the disease is gout.