METTL3 and neoplasm: In both established glioblastoma cell lines and in three different primary cell lines derived from patients, the CRISPR/Cas9-mediated depletion of METTL3 as well as the overexpression of a catalytically inactive dominant negative form of METTL3 in vitrostrongly reduced the proliferation, migration and invasiveness, while increasing the apoptotic index of U87 cells, and in vivo reduced the tumour formation rate.