Growth factors, cytokines, and cell adhesion molecules may regulate oligodendrocyte progenitor (OP) differentiation into remyelinating oligodendrocytes in the environment of a demyelinated lesion. Among these potential signaling molecules, we have examined the in vivo role of endogenous fibroblast growth factor 2 (FGF2), which is upregulated during postnatal development and in acute demyelination (10Y 12). During remyelination after acute demyelination, FGF2 null mice exhibit enhanced oligodendrocyte repopulation of demyelinated lesions (12) . This improved oligodendrocyte regeneration was further studied using in vivo retroviral lineage analysis in wild-type versus FGF2 null mice, which demonstrated that the predominant effect of FGF2 in vivo during remyelination is inhibition of OP differentiation (11) .