It is perhaps significant that any attempt at responsive mitotic activity on the part of neurons as permanent phenotypes might result in injury and loss of cells. Programmed cell death might inherently constitute a component system at promitosis that involves activity on the part of the neuron to enter the cell cycle. It might be in terms of reactivity to inflammation, to trophic factor lack, to ischemia, or to the generation of and exposure to, numerous or varied toxins, that neurons of the anterior spinal horn, brain stem and precentral motor cortex would evolve as promitosis or as induced attempts at mitosis. Promitosis would constitute a susceptibility to cell death in the evolving exposure and development of cell cyclical activity that stresses and damages permanent phenotypic attributes of the neuron. A reactivity on the part of a neuron of specific physiologic category or subclass in amyotrophic lateral sclerosis would induce persistent cell loss that is characterized as aborted cell cyclical activity and as subsequent programmed cell death. Superoxide dismutase activity and its mutant forms would highlight such susceptibility to evolving neuronal injury and stress that is generated as both induced promitosis and as subsequent programmed cell death in the course of repeated attempts at entry into the cell cycle.