We also utilized the K19‐C2mE mice, a spontaneous model of GC that mimics helicobacter‐associated and inflammation‐driven gastric tumorigenesis in patients.[16] We found that knockout of METTL10 in the K19‐C2mE mice led to a reduction in both tumor volume and Ki‐67 expression when compared to their wild‐type (WT) littermates (Figure 1k–m; Figure S1o, Supporting Information). This evidence concerns the gene EEF1AKMT2 and neoplasm.