Our results demonstrate that YULINK inhibition decreased the expression of PDGFR or the activation of PI3K-AKT signaling in PASMCs with PDGF treatment or PAH-PASMCs; furthermore, the inhibition of cell migration and proliferation by LY294002 treatment was significantly reversed in PASMCs with YULINK overexpression or PAH-PASMCs, so the PDGF/PI3K/AKT axis is involved in the effects of YULINK on the pathophysiological development of PAH. This evidence concerns the gene AKT1 and pulmonary arterial hypertension.