The chronic activation of IL-1β has been associated with the development of metabolic syndromes.46 However, postprandial macrophage IL-1β promotes insulin secretion, arguing for a physiological modulating role of IL-1β on whole-body glucose homeostasis.47 Situations associated with chronic inflammation might break the delicate balance on insulin sensitivity and insulin secretion mediated by IL-1β and Nod1 ligands, leading to overt insulin resistance and hyperglycemia. The gene discussed is INS; the disease is metabolic syndrome.