This effect, however, is likely to be independent of NF-κB, given that (a) IKKβ also phosphorylates insulin signaling proteins directly14, (b) overexpression of the active p65 subunit of NF-κB in adipocytes maintains insulin sensitivity in both age-related and diet-induced obesity in mice, despite proinflammatory gene expression in adipose tissue15,16, and (c) mice lacking the regulatory p50 subunit have increased NF-κB activity and yet display resistance to diet-induced obesity and preserved insulin action17,18. The gene discussed is INS; the disease is obesity disorder.