The postulated dependencies include hyperinsulinemia with the activation of insulin-like growth factor (IGF) pathways, co-occurring with obesity, a chronic inflammatory process with the activation of proinflammatory cytokines (TNFα, Il-6, and Il-8), monocyte chemoattractant protein (MCP-1), and the promitogenic role of adipose tissue hormones (mostly leptin) [2, 3]. The gene discussed is LEP; the disease is hyperinsulinism.