Among them, several mitogen-activated protein kinases (MAPKs), including extracellular signal-regulated kinases (ERK1 and ERK2) [47,48], JUN N-terminal kinases (JNK1, JNK2, and JNK3) [49,50,51], and p38 delta [32,33,50,52] were reported to contribute to PAH pathophysiology. This evidence concerns the gene MAPK3 and pulmonary arterial hypertension.