NFKB1 and metabolic syndrome: Thus, it may be hypothesized that higher levels of ROS observed in T2DM, generated by multiple stressors (RAGE and TNF-R signaling, mitochondrial dysfunction, lipotoxicity, etc.), induce apoptosis, while lower ROS concentrations present in MetS engage instead in pathways triggered by the activation of NF-κB, which increases antiapoptotic molecules [81].