In summary, we provide evidence that, in an experimental model of OSA, nmMLCK is a potential molecular target to counteract early stages of atherosclerosis, such as endothelial dysfunction, inflammation through its capacity to increase transendothelial migration of monocytes and, most importantly, through the reorganization of VAMP-dependent vesicles associated with the release of IL-6. The gene discussed is IL6; the disease is endothelial dysfunction.