The proinflammatory kinases JNK1 and IKKβ are activated by almost all the signaling pathways proposed to cause insulin resistance and interference with either JNK1 or IKKβ activity has been found to be protective in lipotoxic conditions and improve insulin signaling in mouse models of obesity and lipid-induced glucose intolerance [23, 24]. The gene discussed is IKBKB; the disease is Glucose intolerance.