Cancers such as multiple myeloma, where NF-κB signaling plays a significant role in the pathogenesis, have been successfully treated with drugs that have NF-κB as their primary or secondary target [38], suggesting that inflammation is a potential target in the search for novel pharmacological interventions to prevent disease progression in CTEPH. Here, NFKB1 is linked to chronic thromboembolic pulmonary hypertension.