In Stage 2, defined by the emergence of metabolic syndrome features such as dyslipidemia, hypertension, and hepatic steatosis, oxidative stress perpetuates low-grade inflammation through redox-sensitive pathways like NF-κB [5,45], while lipid peroxidation and ROS-induced damage impair liver, kidney, and pancreatic β-cell function. This evidence concerns the gene NFKB1 and metabolic syndrome.