In addition, METTL3 deficiency also influences macrophage reprogramming and enhances tumor progression in mouse models, thereby, eliminating the efficacy of PD-1 blockade treatment [26]; mRNA methylation mediated by METTL3/14 sensitizes pMMR-MSI-L colorectal cancer immunity to anti-PD-1 treatment by increasing STAT1 and IRF1 expression in an m6A-dependent manner [25]. This evidence concerns the gene STAT1 and neoplasm.