In adipocytes, disruption of inflammatory genes IKKβ, JNK and IKKε has the potential to promote adiposity and subsequently reverse the obesity-induced insulin resistance [40], [41], [42], while up-regulation of adipocytokines, such as TNFα, IFNγ, IL1, IL6, TGFβ and leukemia inhibitory factor (LIF) has been postulated to inhibit adipogenesis and/or promote lipolysis through regulation of PPARγ. The gene discussed is IFNG; the disease is obesity due to melanocortin 4 receptor deficiency.