MAPK3 and Miller Fisher syndrome: Indeed, we recently reported that H2O2 is produced by neuronal mitochondria in response to acute nerve injuries by neurotoxins or anti-ganglioside and complement complexes, an experimental setting mimicking key pathogenetic events of Miller Fisher syndrome, and engaging the ERK1/2 pathway in perisynaptic Schwann cells (PSCs) at the NMJ [9,34].