These findings suggest that METTL3 and METTL14 are potential therapeutic targets in anticancer immunotherapy Han et al[33] reported that the loss of YTHDF1 in classical dendritic cells enhanced the cross-presentation of tumor antigens and the cross-priming of CD8+ T cells in vivo, and improved the therapeutic efficacy of PD-L1 checkpoint blockade. This evidence concerns the gene CD274 and neoplasm.