Further studies will be required to elucidate not only this molecular function of TRIM67 in developing and adult neurons, but also whether TRIM67 plays a role in DCC-dependent responses, the underlying cause of brain hypotrophy resulting from Trim67 deletion, the changes in cellular structure that lead to fiber tract malformation, the time course of and underlying cause of behavioral abnormalities in Trim67−/− mice, and the contribution of TRIM67 variations to human neurologic disorders. This evidence concerns the gene DCC and nervous system disorder.