Although the molecular mechanisms underlying the TZD effects on PAH development remain unclear, a generally accepted hypothesis is that TZDs may act via their receptor PPARγ to modulate the expression of key genes involved in the pathogenesis of PAH such as ET-1, eNOS, p27KIP1, adiponectin, apoE, MMP, and RhoA/ROCK. This evidence concerns the gene APOE and pulmonary arterial hypertension.