However, the effects of ERK1/2 phosphorylation are considered to be contradictory: both survival and death signals can activate ERK1/2 and therefore activation itself may result in neuronal death or survival.[29] Cellular stress triggers MAPK p38 and JNK activation, for example in the context of cerebral ischemia.[35] It is assumed that p38 and JNK mediated apoptosis is transmitted by mitochondrial pro-apoptotic proteins like Bax and Bcl-2.[35]. The gene discussed is BCL2; the disease is brain ischemia.