ADAM11-deficient mice remained alive for more than one year without ataxia or tremor, but showed a deficit in spatial learning and motor dysfunction. On the other hand, mice lacking the Adam22 gene showed severe ataxia, exhibited marked hypomyelination of the peripheral nerves, and died before weaning [22]. Mice lacking the Adam23 gene showed severe ataxia and tremor and died before weaning [23]. These findings suggest that ADAM11, ADAM22 and ADAM23 have separate and important roles in the nervous system. A genome database search revealed orthologs of ADAM11, ADAM22 and ADAM23 genes to exist in vertebrates such as mammals, fish, and amphibians, but not in invertebrates. Although the precise molecular functions of these ADAMs are still unclear, further investigations will provide clues to understanding the nervous system of higher organisms.