The effects of NFκB-mediated metabolic inflammation are deleterious and can give rise to impairments of normal intracellular signaling and disruptions of metabolic physiology [62] that have been reported also in the CNS—particularly in the hypothalamus—which primarily could account for the development of overnutrition-induced metabolic syndrome and related disorders such as obesity, insulin resistance, T2D, and obesity-related hypertension [68, 75, 76]. This evidence concerns the gene NFKB1 and obesity due to melanocortin 4 receptor deficiency.