IRF9 accelerates the characteristic abnormal proliferation in pulmonary artery smooth muscle cells in PAH by regulating prohibitin 1 (PHB1) expression and leading to mitochondrial dysfunction, including genes linked to endosomes and lysosomal enzymes [58], suggesting that targeting IRF9 may be a novel strategy to delay PAH pathological progression [59], perhaps also through the regulation of HPV E7, which might directly regulate IRF9 expression (Figure 5). Here, IRF9 is linked to pulmonary arterial hypertension.