We chose the RNAi strategy over CF6 antibodies to further determine whether the high CF6 level is a cause or merely an effect of PAH given that a therapeutic antibody should decrease the circulating levels of free CF6 to zero and have a limited duration of effect [33], and especially considering that CF6 signaling proteins have short half-lives. The gene discussed is ATP5PF; the disease is pulmonary arterial hypertension.