Pathophysiological mechanisms underlying LV diastolic dysfunction in OSA have been widely studied: repetitive hypoxemia/re-oxygenation sequences, sympathetic bursts, renin-angiotensin-aldosterone system activation, oxidative stress, systemic inflammation, intra-thoracic pressure reduction and trans-mural pressure increasing, all participate in the development of LV hypertrophy and remodelling, and hence of LV diastolic dysfunction [5–8]. The gene discussed is REN; the disease is obstructive sleep apnea syndrome.