On the other hand, in differentiated cells, activated STAT3, present at both STAT3-binding sites of the GFAP promoter and its exon 1 suggests that a conformational change may bridge both sides of the transcriptional start site during GFAP activation. This conformational change resulted in subsequent recruitment of CBP/p300 to the exon 1 coding region but not the promoter in the ChIP assay. Finally the specific increase of CBP/p300 occupancy at GFAP locus implies that the acetylation by these histone acetyltransferases play roles for gene activation of GFAP. Furthermore, CBP/p300 targeted histone H3 acetylation of the promoter but not exon 1 and induced chromatin remodeling, thereby enhancing recruitment of RNA polymerase II to activate GFAP transcription (Fig. 6 ). In addition, this notion of the change of the acetylation status accompanied with GFAP expression in NTera-2 cells was also supported by another independent assay in which specific HDAC inhibitors were used to increase the acetylated H3K9 and H3K14 in NTera-2 cells (Liao, CH and Yu, J., unpublished observation).