Upon the accumulation of ROS and the elevation of oxidative stress as a result of increased proinflammatory factors and FFAs, the signaling pathways of various stress-sensitive serine/threonine kinases such as IKKβ, are activated and several targets of these kinases including IRS-1 and IRS-2 and the insulin receptor are phosphorylated at serine and threonine sites, resulting in decreased insulin function and insulin resistance [14, 174]. This evidence concerns the gene INS and Insulin resistance.