LC3 exerts protective effects in the pathogenesis of PAH through hypoxia-specific inhibitory effects on the parameters involved in proliferative signaling (MAPK3/ERK1–MAPK1/ERK2 activation, VEGF secretion), as well as the inhibitory effects on pulmonary artery endothelial cells proliferation [86, 87]. This evidence concerns the gene MAPK1 and pulmonary arterial hypertension.