For example, metabolic sensing by immune cells has been recently shown to drive NLRP3-dependent IL-1β release and inflammation in diseases ranging from type II diabetes and obesity to Muckle-Wells syndrome (Kuemmerle-Deschner et al., 2011; Strowig et al., 2012), though the specific mechanisms driving macrophage and NLRP3 activation in these diseases have remained unclear. This evidence concerns the gene IL1B and Muckle-Wells syndrome.