Lipid accumulation in adipose tissue related to obesity activates c-Jun N-terminal kinase (JNK) and nuclear factor kappa B (NFκB) signaling pathways that increase insulin resistance by impairing insulin signaling through serine kinase phosphorylation of insulin receptor substrate (IRS)-1 and by producing proinflammatory cytokines such as TNF-α, IL-6, and IL-1β, which also activate JNK and NFκB pathways all over again [19]. The gene discussed is INS; the disease is Insulin resistance.