We previously found that HDAC1 is a positive transcriptional regulator that drives CD109 gene expression via a protein complex formation with an oncogenic TF C/EBPβ,16 even though HDAC1 is recognized to modulate the compact chromatin structure leading to widespread repression of transcriptional activities in cancers and developmental somatic cells.38–40 It remains unknown if PLAGL1 forms a larger protein complex with HDAC1 and C/EBPβ in glioblastoma and other cancers. This evidence concerns the gene TF and glioblastoma.