As such, synaptically released dopamine can be cleared by oxidation via MAO-B, and pharmacological modulation of MAO-B with rasagiline, selegiline or safinamide has been shown to increase synaptic dopamine concentrations, thus rendering them useful as an adjunct to levodopa therapy, and also as early-stage monotherapies in PD [246–249]. The gene discussed is MAOB; the disease is Parkinson disease.