As to how countering effects of elevated MAO-A protein could have longer lasting benefit, preventing monoamine deficits could be helpful since monoamine depletion, whether by reduction of serotonin precursor tryptophan,8 inhibition of tyrosine hydroxylase through administration of α-methyl-p-tyrosine9 or removal of all three by disruption of vesicular storage via reserpine10 leads to depressive syndromes, with the latter occurring after substantial time delay. The gene discussed is TH; the disease is depressive disorder.