The Authors

2 Olig1 is a basic helix-loop-helix (bHLH) transcription factor expressed in cells of the oligodendrocyte lineage in the nervous system. Its role during normal development has not yet been fully resolved, but it is known that in adult life the protein is crucial in the process of remyelination after injury.[1][2][3] Olig1 translocates from the cytoplasm to the nucleus in early remyelinating lesions in rodent models of demyelinating disease as well as in oligodendrocyte precursor cells at the edge of multiple sclerosis (MS) lesions.[1] Olig1 specifically regulates the expression of the major myelin-specific genes during oligodendrocyte maturation in the brain,[2] and remyelination after injury is impaired in Olig1−/ − mice.[1] In patients with MS, remyelinating capacity is limited even though oligodendrocyte precursor cells are often efficiently recruited.[4] These findings raise the question whether genetic variants in the Olig1 gene (Olig1) influence remyelinating capacity and vulnerability to the consequences of a demyelinating event.[5] In order to investigate this hypothesis, we first aimed at identifying any Olig1 codin