Mutations in histone H3 have been proven by Capdevielle et al. to be oncogenic drivers in diffuse midline glioma, and targeting this epigenetic abnormality by HDAC inhibitors is a potential therapeutic regimen for diffuse midline glioma treatment through regulating scaffolding proteins EBP50 and IRsp53 (14). Here, BAIAP2 is linked to diffuse midline glioma.