Multiple sclerosis, a typical demyelinating disease, and cerebral ischemia associated with stroke cause white matter injury. Oligodendrocytes, one of the glial cells, are responsible for remyelination at the site of white matter injury. However, the remaining unregenerated areas of white matter lesion inhibit functional recovery. This study aims to elucidate the mechanism of remyelination failure in these white matter lesions and to develop new therapeutic strategies targeting regeneration inhibitors.