Another example for indirect proof of an uncoupled eNOS was reported in the animal model of deoxycorticosterone acetate salt hypertension (Landmesser et al, 2003), showing the impaired •NO synthesis by a decreased EPR-NO-signal and the increase of eNOS activity in response to supplementation with BH4 or by genetic deletion of the NADPH oxidase subunit p47phox (removing the “kindling radical” for NOS uncoupling). This evidence concerns the gene NCF1 and Hypertension.