It was reported that depletion of Mettl3 or Mettl14 in CRC cells enhanced the response of Patient-Derived Xenograft (PDX) mice to anti‐PD‐1 treatment by stabilizing the STAT1 and IRF1 mRNA and promoting IFN‐γ‐Stat1‐Irf1 signaling, which recruited cytotoxic tumor‐infiltrating CD8+ T cells in tumor microenvironment with escalated IFN‐γ, Cxcl9 and Cxcl10 51. The gene discussed is METTL3; the disease is neoplasm.