ER stress and the UPR lead to obesity-induced inflammation and metabolic abnormalities by several distinct mechanisms, including the activation of JNK-AP1 (Jun N-terminal Kinase-Activator Protein 1) and IKK (IκB kinase)-NFκB pathways, the induction of the acute-phase response, and the production of reactive oxygen species (ROS) [34, 35]. This evidence concerns the gene NFKB1 and obesity disorder.