Metabolically active visceral adipose tissues produce inflammatory mediators and cytokines (e.g., TNF-α and leptin), inhibit adiponectin secretion, and facilitate the development of insulin resistance and subsequent hyperinsulinemia, promoting carcinogenesis partly by stimulating an increase in insulin-like growth factor 1 (IGF-1) expression [43]. This evidence concerns the gene LEP and Hyperinsulinemia.