The expression of phosphorylated SMAD2/3 proteins was markedly enhanced upon R428 treatment, indicating that Axl inhibition on PAH is linked with a switch between TGF-β-SMAD2/3 and BMPR2-SMAD1/5/8 signaling (Fig. 5e, f). The gene discussed is SMAD1; the disease is pulmonary arterial hypertension.