Rescue of nigral Akt activity in HF animals by viral overexpression of insulin receptor substrate 2 (IRS2) restored striatal DAT surface expression and DA clearance, and reduced hyperphagia, while pharmacological inhibition of Akt in normal rats blunted DAT activity, supporting a causal link between impaired insulin signaling and striatal DAT activity [8]. The gene discussed is AKT1; the disease is hydrops fetalis.