For example, IL-1β, IL-6 and TNF-α have been shown to contribute directly to insulin resistance by activating stress kinases, such as IκB kinase (IKK), c-Jun N-terminal kinases (JNKs) and the P38 mitogen-activated protein kinases (MAP38) in muscle and fat cells, which inhibit the function of the insulin receptor (IRS1), thus blocking signal transduction [47,48]. This evidence concerns the gene INSR and Insulin resistance.