Furthermore, truncating mutation in CAV1 causes the excessive phosphorylation of SMAD1, SMAD5, and SMAD9, which leads to the decrease in the antiproliferative function of caveolin-1, thus demonstrating that functional gain SMAD may be one of the potential molecular mechanisms of CAV1-associated PAH (Marsboom et al., 2017). This evidence concerns the gene CAV1 and pulmonary arterial hypertension.