DPYSL2 and amyotrophic lateral sclerosis: We are currently exploring the development of LKE and related molecules as novel neurotrophic factors for ALS axonopathy and other indications, but this early data clearly suggests that (1) CRMP2-targeting signal transduction pathways are plausible candidates to explain the noncell autonomous, distal axonopathy component of ALS and (2) these signaling pathways are amenable to deliberate pharmacological intervention.