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We have previously shown that levels and activity of non\u2010muscle myosin II (NMII), a regulator of cytoskeletal contractility, decrease as a function of differentiation and that inhibition of NMII increases branching and myelination of OL in coculture with neurons. We have also found that mixed glial cell cultures derived from NMIIB knockout mice display an increase in mature myelin basic protein\u2010expressing OL compared with wild\u2010type cultures. We have now extended our studies to investigate the role of NMIIB ablation on myelin repair following focal demyelination by lysolecithin. To this end, we generated an oligodendrocyte\u2010specific inducible knockout model using a Plp\u2010driven promoter in combination with a temporally activated CRE\u2010ER fusion protein. Our data indicate that conditional ablation of NMII in adult mouse brain, expedites lesion resolution and remyelination by Plp+ oligodendrocyte\u2010lineage cells when compared with that observed in control brains. Taken together, these data validate the function of NMII as that of a negative regulator of OL myelination <jats:italic>in vivo<\/jats:italic> and provide a novel target for promoting myelin repair in conditions such as multiple sclerosis. 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