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In an elegantly presented series of experiments, Tagami et al. demonstrate that transcorneal electrical stimulation increases retinal ganglion cell (RGC) axonal regeneration and survival after optic nerve crush in the rat. They show that this effect is mediated by insulin growth factor 1 (IGF-1), based on abrogation by the cyclic peptide IGF-1 antagonist JB3. Appropriate anterograde and retrograde labeling techniques were used to identify RGC axons and somata, respectively. Although the magnitude of observed regeneration was not great, from a mechanistic perspective this opens up an exciting area for future exploration. Perhaps the most intriguing is the signaling mechanism which connects electrical stimulation to IGF-1 expression. One possibility is low-level injury, similar to a preconditioning stimulus, mediated by current flow via M�ller cells. Another might be effects on the lens, or induction of subclinical inflammation. Although it is difficult to directly extrapolate these results to the diseased human eye, these data are still exciting and innovative.