In patients suffering from the obstructive hypoventilation syndrome (OHS), the most severe form of sleep-disordered-breathing, we found that circulating exosomes contributed to the induction and propagation of OSA/OHS-related endothelial dysfunction (i.e., increased permeability and disruption of tight junctions along with increased adhesion molecule expression and reduced endothelial nitric oxide synthase expression) and promoted increased monocyte adherence [65]. This evidence concerns the gene NOS3 and sleep apnea syndrome.