The histopathology of PH is characterized by arteriolar intimal proliferation, evolving to aspects of concentric or eccentric laminar sclerosis, medial hypertrophy and adventitial proliferation, with variable inflammatory reactions and occasional aspects of fibrinoid necrosis.[24] The aberrant proliferation of PASMCs is a significant inducer for medial hypertrophy, which is partially triggered by endothelial dysfunction.[3] Thus, whether SOX17‐associated exosomes regulate the proliferation of PASMCs in a paracrine manner was also analyzed. This evidence concerns the gene SOX17 and endothelial dysfunction.