It was proposed that this improved efficacy is based on the mechanism, which the depletion of METTL3 and METTL14 causes the stabilization of STAT1 and interferon regulatory factor 1 (IRF1) mRNA via YTHDF2, leading to interferon (IFN)-γ signaling and increased numbers of cytotoxic tumor-infiltrating CD8+ T cells in vivo. The gene discussed is STAT1; the disease is neoplasm.