The state of chronic intermittent hypoxemia and the altered microenvironment in OSA patients, such as the increase in IL-6 levels and reduction in TGF-β levels, could damage the function of endothelial cells and promote a Th17/Treg imbalance, which leads to a reduction in the production of endothelium-dependent vasodilator substances and contributes to vascular dysfunction and stimulation of systemic inflammation (63–67). The gene discussed is TGFB1; the disease is obstructive sleep apnea syndrome.