Activation of the Ras homolog gene family, member A (RhoA) GTPase and it downstream effector, the Rho-associated kinase (ROCK), have been implicated in several processes driving PAH pathogenesis, including SMC vasoconstriction and proliferation, and endothelial cell contraction (Oka et al., 2008). This evidence concerns the gene RHOA and pulmonary arterial hypertension.