Current studies suggest that the acute flares of gout depend on two switches, one of which is the activation of the TLR2/4-NF-κB signaling pathway within macrophages or monocytes, which promotes the synthesis of pro-IL1-β and significant components of the inflammasome, and that this activation is associated with the influence of large amounts of free fatty acids, intestinal flora or other microorganisms (32, 33). Here, IL1B is linked to gout.