Firstly, NF-κB is the key inflammatory transcription factor well known to be activated by oxidative stress[33] which is implicated in human[21] and experimental PAH[17]; its activation leads to the upregulation of chemokines and inflammatory cytokines implicated in human IPAH[34] and in the MCT-induced PH model where its inhibition ameliorates PH - both preventatively and therapeutically[35,36]. This evidence concerns the gene NFKB1 and pulmonary arterial hypertension.