In summary, several lines of evidence presented in this study clearly support the activation of JNK3 in vitro in an MPP+-induced cellar model of PD and that the cell-permeable JNK3-N-Tat peptide inhibits this activation by disrupting the binding of β-arrestin2 to the N-terminus of JNK3, thereby exerting protective effects against MPTP-induced dopaminergic neuronal toxicity. The gene discussed is TAT; the disease is Parkinson disease.