Mechanistically, Mettl3-deficient mice showed increased M1/M2-like tumor-associated macrophage and regulatory T (Treg) cell infiltration in the local tumor microenvironment due to the impairment of YTHDF1-mediated SPRED2, which enhances the activation of nuclear factor κB (NF-κB) and STAT3 via the ERK pathway and consequently leads to tumor growth and metastasis. This evidence concerns the gene SPRED2 and neoplasm.