In the pulmonary hypertension paper [1], it was shown that two causal factors of that disease, endothelin-1 (ET-1) and RhoA (acting through Rho kinases), both function as NO/ONOO-cycle elements: That is they are each raised in response to NO/ONOO-cycle elements and they each raise NO/ONOO-cycle elements. This evidence concerns the gene EDN1 and pulmonary arterial hypertension.