The overexpression of IL-18 in the lungs resulted in mild PAH and RV dilation, but the genetic ablation of IL-18 did not attenuate hypobaric hypoxia-induced PAH and right ventricular hypertrophy [44], suggesting that IL-18 may be a disease modifier, but it is not the causal factor for PAH development. The gene discussed is IL18; the disease is pulmonary arterial hypertension.