This is caused through defects in the metabolic pathway of insulin receptors, mammalian target of rapamycin (mTOR), and ribosomal protein S6 kinase beta-1 (S6K1) with an increase of proinflammatory proteins, endothelial dysfunction, the renin-angiotensin system, and dyslipidemia [44]. The gene discussed is INSR; the disease is endothelial dysfunction.