In a mouse model, knockout of PPAR-γ resulted in spontaneously developed PAH and RV hypertrophy (108), whereas its activation by rosiglitazone, a widely acknowledged PPAR-γ agonist used in the treatment of diabetes, has prevented the development of PAH induced by hypoxia (61) or hyperoxia (62). This evidence concerns the gene PPARG and pulmonary arterial hypertension.