Equally, the m6A “eraser” ALKBH5 controls the demethylation of PD-L1 mRNA; loss of ALKBH5 destabilizes PD-L1 transcripts via enhanced YTHDF2 binding, increasing tumor vulnerability to T-cell–mediated lysis and potentiating responses to PD-1 blockade in preclinical glioblastoma models (5). This evidence concerns the gene CD274 and neoplasm.