However, an increase in Acvr2b+ oligodendroglial lineage cells was observed in non-repairing white matter (injured regions following perinatal brain injury, and chronic inactive multiple sclerosis lesions), which would be predicted to sequester ligand and consequently impair Acvr2a-regulated oligodendrocyte differentiation and myelin formation. The gene discussed is ACVR2A; the disease is injury.