Our results show that diabetes induces oxidative–nitrosative stress in the diabetic parotid gland as well as in diabetic dental pulp [3], reflected by increased iNOS expression and enhanced total SOD activity, and that accompanied GDNF upregulation may be a mutual nitrosative stress-responsive mechanism, given the strong positive correlation between iNOS and GDNF presently observed under diabetic conditions. The gene discussed is SOD1; the disease is diabetes mellitus.