One plausible molecular mechanism for obesity-associated carcinogenesis is that visceral adipose tissue, which is metabolically active, promotes the release of inflammatory cytokines and mediators, including free fatty acids, tumor necrosis factor α (TNFα), leptin, and resistin, inhibits the secretion of adiponectin and ultimately leads to development of insulin resistance [8,9,57]. This evidence concerns the gene LEP and obesity due to melanocortin 4 receptor deficiency.