In dysfunctional AT, there is an imbalance between proinflammatory and anti-inflammatory factors, specifically an increase in proinflammatory adipokines, such as IL-1 β, IL -6, IL-18, resistin, tumor necrosis factor α (TNF-α), and leptin, and a decrease in anti-inflammatory adipokines such as IL-10, secreted frizzled-related protein 5, nitric oxide (NO), and adiponectin, perpetuating an environment of low-grade chronic inflammation more prone to atherogenic repercussions [33,35,36]. This evidence concerns the gene TNF and inflammatory response.