Importantly, PDK may be induced selectively by activation of HIF-1 α and PDH may be inhibited by inhibition of SIRT3, both of which are biochemical events that define PAH.19 These collective observations and other related lines of empiric investigations in cellulo and in vivo gave rise to the hypothesis that dichloroacetate (DCA), which inhibits PDK (and, thus, removes negative inhibition of PDH by PDK), may be useful clinically. This evidence concerns the gene PDP1 and pulmonary arterial hypertension.