This can be explained as follows: the excess abdominal fat in central obesity facilitates insulin resistance by secreting various substances such as inflammatory cytokines (e.g., TNF-α and IL-6), free fatty acids (FFAs), and adipokines (e.g., adiponectin and resistin), leading to inflammation, glucose intolerance, and hyperglycemia [49]. The gene discussed is TNF; the disease is Glucose intolerance.