 The structure of this cleaved form of CRMP has not been determined yet, making it difficult to understand the protein-protein interactions that occur and why these forms are able to initiate neurodegeneration after CNS injury.Additionally, calpain inhibitors (ALLN) are shown to have prevented the CRMP‐3 cleavage and therefore no axonal degeneration or neuronal death, further suggesting that calpain targets CRMP-3 for cleavage during glutamate-induced neuronal death.Ca2+/calmodulin-dependent protein kinase II (CaMK II) is also activated by calcium influx through NMDA receptors, and is another possible activator of CRMP-3.