However, only a few clinical studies have shown associations between FGF23, α-klotho and various indexes related to T2DM, including insulin resistance (measured by homeostasis model assessment of insulin resistance), dyslipidemia, resistin levels, and obesity status, suggesting that an imbalance in the FGF23/α-klotho axis may result in an unfavorable lipid profile, which could contribute to the development or progression of both T2DM and atherosclerosis [31–33]. This evidence concerns the gene KL and type 2 diabetes mellitus.