The link between OSA and cardiovascular diseases can be attributed to the fact that occasional episodes of hypoxemia and hypercapnia lead to increased sympathetic activity, heart rate variability, and arterial tension, and consequently, induce the production of vasoactive substances (catecholamines) and inflammatory mediators (interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), macrophage inflammatory protein-2 (MIP-2), cyclooxygenase-2 (COX-2), and C-reactive protein (CRP)) [3,4]. This evidence concerns the gene IL1B and obstructive sleep apnea syndrome.