However, growing evidence implicates a role for Noxs, particularly Nox1 and Nox4, in the development and progression of PAH.39,40 We found increased basal levels of Nox1 and Nox4 in PAH-hPASMCs compared with control hPASMCs in agreement with other studies.18,40 16αOHE1 induced an increase in expression of Nox1 and Nox subunits associated with Nox1 activation, whereas Nox4 and its regulator poldip2 were not significantly modified in PAH-hPASMCs. The gene discussed is POLDIP2; the disease is pulmonary arterial hypertension.