However, the aforementioned research papers did not consider potential interactions of the AR index in the development of MetS for patients who already present T2DM and did not provide a study design that prospectively included adiponectin and resistin independently in several time cycles, enhancing the AR index’s ability to reflect the balance of adipokine-mediated effects on insulin sensitivity in terms of MetS and T2DM pathogenesis. The gene discussed is RETN; the disease is metabolic syndrome.