(52) demonstrated that the specific knockdown of Mettl3 in the myeloid cells of mice (crossed Mettl3fl/fl mice with Lyz-cre mice to delete Mettl3) leads to tumor progression by promoting the accumulation of M1/M2-like tumor-phenotype macrophage and facilitating the infiltration of regulatory T cell (Treg) into tumors. This evidence concerns the gene METTL3 and neoplasm.