Evidence to date suggests that these roles are mainly related to STAG1-cohesin [reviewed in (4)] and indeed, repair of inactivating STAG2 mutation to generate normal expression in glioblastoma cells was recently reported to have no significant effect on the transcriptional profile, suggesting that the role of STAG2 may be restricted to its functions in chromatid cohesion (1). Here, STAG1 is linked to glioblastoma.