In addition to oxidative stress, several core mechanisms may participate in MetS programming [45], including the glucocorticoid effect [123], dysregulated nutrient-sensing signals [124], aberrant activation of the renin–angiotensin aldosterone system (RAAS) [125], gut microbiota dysbiosis [126], etc. Oxidative stress acts a molecular hub facilitating a wide range of functional interactions among the above-mentioned core mechanisms behind MetS programming (Figure 2). This evidence concerns the gene REN and metabolic syndrome.