Nevertheless, based on previously discussed dependence of Cav-2 protein stability and plasma membrane lipid raft/caveolar targeting on Cav-1, it is possible that reduction/loss of Cav-2 rather than Cav-1 could be more directly responsible for hyperactivation of the STAT3 pathway, increased expression of cyclins D1 and D3, and pulmonary hypertension in mice and possibly rats with chemically-induced pulmonary hypertension. The gene discussed is CAV1; the disease is pulmonary arterial hypertension.