In addition, Michelakis et al found that DCA administration activated PDH and increased mitochondrial respiration, resulting in lower mean pulmonary artery pressure and pulmonary vascular resistance in patients with idiopathic PAH in a 4-month clinical study.[67] This is the first human trial of DCA in patients with idiopathic PAH, which suggests that PDK is an efficient target for PAH therapy. This evidence concerns the gene PDP1 and pulmonary arterial hypertension.