Moreover, Cirp knockdown enhanced the permeability of FITC‐dextran and release of LDH, which could be inhibited by Cav1 or Cavin1 overexpression, further confirming the functional role of CAV1 and CAVIN1 in CIRP‐dependent endothelial cell apoptosis and permeability, suggesting CAV1 and CAVIN1 are downstream targets of CIRP in PAH. This evidence concerns the gene CAV1 and pulmonary arterial hypertension.