In addition, palmitate, a free fatty acid known as a key mediator of obesity-induced inflammation, induces the production of the proinflammatory cytokine TNF-α without activating the canonical NF-κB pathway14, indicating that although NF-κB activation is required for obesity-induced inflammation, it may be independent of canonical IKKβ-dependent IκBα degradation. The gene discussed is TNF; the disease is obesity due to melanocortin 4 receptor deficiency.