Intrinsic programs regulating cell fate determination of progenitors include epigenetic modifications such as DNA methylation and chromatin remodeling. Methylation of the STAT-binding element within the glial fibrillary acidic protein (GFAP) promoter in mice was shown to inhibit the association of activated STATs with the glial promoter, thereby repressing transcription of the GFAP gene [10, 16, 21] . Furthermore, conditional deletion of the maintenance DNA methyltransferase I from neural progenitor cells (NPCs) suggests that DNA methylation regulates the timing and magnitude of astrogliogenesis [22] . Another class of epigenetic modifications was found from FGF2, which regulates the ability of ciliary neurotrophic factor to enhance astrocyte differentiation by inducing H3 Lys4 dimethylation and suppressing H3 Lys9 dimethylation at the STAT3-binding site, resulting in access of the STAT/CBP complex to the GFAP promoter and activation of GFAP expression [16] . Those reports highlight the diverse epigenetic mechanisms that control lineage-specific gene expression; however, it remains unclear how the interplay among DNA methylation, transcriptional repressors or activators, and histone modifications contributes to regulation of the processes.