In searching for the mechanisms involved in inflammation-induced insulin resistance, SOCS proteins [104,105], endoplasmic-reticulum (ER) stress [106], the inhibitor of nuclear factor-κB (NF-κB) kinase-β (IKKβ) of NF-κB activation and the JUN N-terminal kinase (JNK) signaling pathways have been all associated with the development of insulin resistance. This evidence concerns the gene NFKB1 and Insulin resistance.