IPAH patients with BMPR2 mutations have significantly more exosomes released from blood outgrowth ECs (BOECs) and contain more TCTP, which is transferred to pulmonary arterial smooth muscle cells (PASMCs), decreases caspase-3 activity and contributes to cell resistance to apoptosis (186). The gene discussed is BMPR2; the disease is idiopathic pulmonary arterial hypertension.