In fact, IL-32 has been described in the abnormal ECs, populating the plexiform lesions in the lungs from iPAH patients [25], and its production seems to promote the leukocyte recruitment via the production of pro-inflammatory cytokines, such as tumour necrosis factor-α (TNF-α), IL-1β, IL-6 and IL-8 [27], all contributing to EC injury [24, 25, 31]. Here, CXCL8 is linked to idiopathic pulmonary arterial hypertension.