These enrichments were preferentially associated with the MS‐like subtype and revealed that the transcription factors BATF3, members of the AP‐1 complex (FOS, FOSB, FRA1‐FOSL1 and FRA2‐FOSL2, JUNB), members of the CEBP family (CEBPA, CEBPB), HOXA9, SMAD3 and RUNX‐related factors (RUNX1, RUNX2) played an important role in the modulation of the epigenomic landscape of the most aggressive GBM subtype (Fig. 3D). The gene discussed is SMAD3; the disease is glioblastoma.