If the positive feedback between Akt and TGF-β is present in the neuronal systems altered in PD, it is possible that defective Akt activation by insulin resistance may reduce TβRI and TβRII exposure at the cell surface, leading to deficient TGF-β/Smad3 signalling and the pathological signs related to parkinsonism. The gene discussed is AKT1; the disease is Insulin resistance.