In obesity, excessive visceral fat accumulation causes adipose tissue dysfunction that leads to chronic-low grade inflammation with adipocyte hypertrophy and hyperplasia, shift from a type 2 to type 1 cytokine-associated inflammatory environment, altered secretion of adipokines (leptin, adiponectin, and other), and changes in proportions and kind of immune cells toward pro-inflammatory monocytes and Th17 lymphocytes, which strongly contributes to obesity-related comorbidities [3–5]. This evidence concerns the gene LEP and obesity disorder.