JAK2/STAT3 pathway can be activated by several pro-fibrotic and pro-inflammatory factors such as TGFβ1, PDGF, vascular endothelial growth factor (VEGF), IL-6, IL-13, angiotensin II (AT2), 5-hydroxytryptamine (5-HT), and endothelin 1 (ET-1), all of them activated in IPF and Pulmonary hypertension (PAH) and involved in the development of pulmonary vasoconstriction (the case of 5-HT, ET-1, and AT2) [34]. Here, JAK2 is linked to idiopathic pulmonary fibrosis.