Hypothalamic overexpression of a constitutively active IKKβ isoform (which is activated by saturated fatty acids and oxidative stress) can reduce both insulin and leptin signaling151; conversely, intracerebroventricular administration of an IKKβ inhibitor reverses high fat diet‐induced hypothalamic insulin resistance,157 and neuron‐specific deletion of IKKβ maintains leptin and insulin sensitivity in high fat diet fed mice.151. The gene discussed is INS; the disease is Insulin resistance.