In comparison to the L-NNA treatment, the double mutant (A53T -/+; nNOS-/+) experiment supports the notion that the contribution of the nitrosative stress in the PD is not just depending on nNOS, but also possibly involving the activity of eNOS and iNOS as we know that different NOS activity can affect the pathogenesis of PD from previous studies [53, 54]. The gene discussed is NOS1; the disease is Parkinson disease.