On the other hand, PDE5A has been reported to be critically involved in cardiovascular diseases and cardiopulmonary disorders,[41, 42] including pathological cardiac hypertrophy,[43] pulmonary hypertension,[44] and abdominal aortic aneurysm.[45] Here in our study, we further demonstrated that overexpression of MTDH or PDE5A could block the protective effect of miR‐30d against hPASMC proliferation and migration, providing direct evidence that MTDH and PDE5A act as downstream targets mediating the functional role of miR‐30d in hPASMC. The gene discussed is MTDH; the disease is pulmonary hypertension.