Since the DJ-1 mutations have been linked to familial PD and hypersensitivity to toxins that induce oxidative stress [23], we examined a signaling pathway that controls oxidative stress responses by DJ-1 in Drosophila. We demonstrated that DJ-1β inhibits oxidative stress-induced neuronal apoptosis by regulating DLP gene expression and protein subcellular localization, suggesting a causal relationship between DJ-1β mutation and oxidative stress-induced DA neuronal loss in PD. This evidence concerns the gene TXNL4B and Parkinson disease.