Possibly, this might be the release of the NO by its own [61,62,63], activated phosphorilazation of eNOS [53] as a special modulatory effect, given the mentioned counteraction of the adverse effect of NOS-blockade (i.e., L-NAME-hypertension and pro-thrombotic effect), as well as the counteraction of the adverse effect of NOS-over-stimulation (i.e., L-arginine-hypertension and anti-thrombotic effect) [58,62]. The gene discussed is NOS1; the disease is Hypertension.