Smad3 deficiency, a molecule involved in the intracellular TGF-β1 signaling cascade, provides us with a new and interesting model of PD, as it promotes selective postnatal neurodegeneration of dopaminergic midbrain neurons, strong MAO-mediated catabolism of DA in the striatum and oxidative stress, as well as dampening the trophic and astrocytic support to dopaminergic neurons. The gene discussed is SMAD3; the disease is Parkinson disease.