IL‐1β and NLRP3 activation are well characterised in a number of non‐communicable diseases involving sterile inflammation including gout,8 atherosclerosis9 and type II diabetes (T2D).10, 11 Neuroinflammation caused by microglial activation is also often dependent on NLRP3 and IL‐1β and is associated with depression12 and Alzheimer's disease (AD).13, 14 Gain‐of‐function mutations in the NLRP3 gene causes spontaneous IL‐1β release in patients with cryopyrin‐associated periodic syndrome (CAPS) diseases that are characterised by fever, rashes and extensive joint pain.15 This evidence concerns the gene NLRP3 and gout.