Because in neuroblastoma and in myeloma p53 is a key SETD8 substrate [10, 11], to contextually address if p53 has a role in mediating SETD8 activity also in glioblastoma, we choose LN-18 cells, in which p53 transcriptional activity is preserved, and U251 cells, in which p53 transcriptional activity is lost [12, 13]. Here, KMT5A is linked to glioblastoma.