Consequently, it is possible that the anti-tumoral effect of KMT5B observed in our study would not be due to the overexpression of this epigenetic modifier itself, but rather might be mediated by the re-establishment of levels of its product H4K20me2 in the promoter region of key GBM-related genes, such as IL13RA2 and CDH11. This evidence concerns the gene CDH11 and glioblastoma.