YTHDF1 and neoplasm: While tumor-intrinsic YTHDF1, a versatile and powerful m6A reader, was demonstrated to drive immune evasion and resistance to immune checkpoint inhibitors via promoting MHC-I degradation, an exosome-mediated CRISPR/Cas9 system was shown to introduce YTHDF1 deficiency and restore expression of MHC-I and tumor immune surveillance [230].