Since the ASK-1/MKK3/6/p38 MAPK pathway is specifically responsible for triggering apoptotic cell death and neuronal loss in PD, it will be important to precisely identify downstream targets of p38 MAPK that are activated upon EtBr exposure that are essential for survival in EtBr, so that pharmacological intervention to enhance the activity of those genes can slow down or improve pathogenesis of PD and other mitochondrial diseases. This evidence concerns the gene MAP3K5 and inborn mitochondrial metabolism disorder.