The activation of NF-κB in MCT-PAH leads to disruption of the BMPR2–ID–Notch3 axis, amplification of the inflammatory response, increased cell death in PAECs, and promotion of EndMT.356 This process also promotes TGF-β-induced EndMT and is associated with increased expression of inflammatory factors, including IL-1β, IL-6, and TNF in MCT-PAH mice.356. Here, IL1B is linked to pulmonary arterial hypertension.