Further Western blot analysis revealed that the PAH rodents group, in contrast to the control group, had an elevated phosphorylated state of AKT (p-AKT/AKT), a crucial effector that responds to various growth factors, as well as upregulated phosphorylation of FOXO3A (p-FOXO3A/FOXO3A) (Figure 6C–G and Figure 7C–G), resulting in cell proliferation in the pulmonary artery, which is regarded as a prominent mechanism in the development of PAH. Here, FOXO3 is linked to pulmonary arterial hypertension.