The main hemodynamic determinants known to produce pulmonary hypertension in hyperthyroidism are increasing levels of thyroid hormones, pulmonary vascular resistance and high cardiac output.2-4 The excess of thyroid hormones leads to the increase of cardiac contractility, the increase of cardiac flow and of systolic pressure blood and decreases the systemic vascular resistance.2-4 The rise of CO is itself determined by the increase of HR and LVEF as an effect of the direct and indirect action of thyroid hormones and hyper-sympatheticotonia. The gene discussed is TG; the disease is pulmonary hypertension.