Moreover, p53 mutants can interact with supervillin (SVIL) and recruit the H3K4me3 methyltransferase MLL1, activating the expression of YTHDF2 N6-methyladenosine (m6A) reader, hampering the expression of m6A-marked tumor-suppressing transcripts and supporting gliomagenesis [67]. The gene discussed is TP53; the disease is neoplasm.