This interaction can cause the activation of MAPK and PI3K pathways in the immune cells, enhancing the proinflammatory mediators’ production, such as tumor necrosis factor alpha (TNF-α), interleukin (IL)-1 and IL-6 that are some of the most important inflammatory mediators that sustain the process of systemic inflammation linked to the metabolic syndrome [19]. The gene discussed is TNF; the disease is inflammation.