Investigations on why hypomyelinogenesis occurred in ADAM22-deficient mice centre on integrin. This is because several ADAMs have been shown to interact with integrins via disintegrin domains [9], and it has been suggested that alpha-6 beta-1 integrin on the Schwann cell plays an important role in myelin formation [25]. In addition, laminin-2 is a key player in peripheral myelin formation, because laminin-2 deficiency causes dysmyelination in mice and humans, and its receptors, alpha-6 beta-1 integrin and dystroglycan, are also shown to be deeply involved in myelin formation [26,27]. The conditional knockout studies of beta-1 integrin and laminin gamma-1 in Schwann cell suggested that both laminin-2 and integrins are essential for segregation of large bundles of axons in the early stage of myelin formation [25,28]. In contrast, the phenotype seen in the ADAM22-deficient mice was quite different: for example, unsorted bundles of axons were not seen in nerves and roots. We assume that ADAM22 partially modulates integrin-mediated signals or is involved at a later stage of myelin formation.