TLR signalling via the NLRP3 inflammasome has been implicated in gout susceptibility and pathology in vivo and in vitro [10]; for example, MSU uptake and IL-1β production by bone marrow-derived macrophages derived from TLR2, TLR4 or Myd88 knockout mice is significantly reduced, as is neutrophil influx, in response to subcutaneous injection of MSU in whole animals [18]. The gene discussed is IL1B; the disease is gout.