The pathophysiological link between obesity and AT remains largely unclear, however growing evidence points to reduced immunological tolerance secondary to an altered balance of adipokines (e.g., leptin and adiponectin) and cytokines [e.g., interleukin 6 and TNF-α) produced by the white adipose tissue and resultant abnormalities of the immune response (47). The gene discussed is LEP; the disease is obesity disorder.