It demonstrates that p38 MAPKα is implicated in the pathogenesis of pulmonary hypertension and administration of selective p38 MAPK inhibitors in vivo demonstrated that the pulmonary hypertensive phenotype cannot only be prevented, but reversed, with improvements in PVremod, acting through inhibition of key inflammatory mediators such as IL-6. This evidence concerns the gene IL6 and pulmonary arterial hypertension.