At this point, it is important to recall the pathophysiological hypotheses concerning CMS: depressed ventilation, especially during sleep (aggravated by sleep apnea and overweight), severe hypoxemia, increased secretion of erythropoietin, and excessive erythrocytosis (Richalet et al., 2008; Villafuerte and Corante, 2016); CMS is sometimes associated with pulmonary hypertension due to chronic hypoxic remodeling of the pulmonary vasculature (León-Velarde et al., 1994). The gene discussed is EPO; the disease is Sleep apnea.