Epigenetic modifications of histone proteins play a crucial role in the activation or repression of genes in proliferating and differentiating neural stem cells (NSCs). The chromatin structural proteins High mobility group B protein (HMGB2) has been shown in some species to influence modifications of histone H3. Moreover we have previously shown that loss of HMGB2 in mice results in aberrant proliferation of NSCs. The purpose of the current study was to identify the effect of HMGB2 loss on histone modifications. We used mouse embryonic fibroblast lines (MEFs) established from wild type and HMGB2 knockout mice in these experiments. We looked at a possible role of bivalent domains - H3K4me3 (a transcriptional activator) and H3K27me3 (a transcriptional repressor) in the proliferation and differentiation of NSCs. We identify potential modifiers of transcription that may interact with HMGB2. Chd1 is a helicase that recognizes H3K4me3 and potentially binds HMGB2 in our MEF culture system, and we are exploring a potential interaction between the two factors and via Co-IP experiments. The outcome of our study will provide insight into the role of HMGB2 in the epigenetic programming of NSCs.