PARP1 and myeloid sarcoma: Nevertheless, previous studies have shown that excessive PARP1 activation mediates acute neuronal death after focal cerebral ischemia,[156] neurotrauma,[10] and in response to reactive oxygen (nitrogen) species‐induced CNS injury[157] and glutamate‐mediated excitotoxicity.[83, 158] These published data provide some clues for future studies testing the function of PARP1 in neuronal/axonal pathology in the context of MS and EAE.