In YTHDF2-deficient cells, re-expression of wild-type YTHDF2 but not the catalytically inactive mutant offset the acquired cancer-promoting inflammatory phenotypes (Fig. 5a, b), and reduced both phosphorylation of STAT3 and stabilization of IL11 and SERPINE2 mRNAs (Fig. 5c-e and Additional file 1: Figure S6C, D). This evidence concerns the gene STAT3 and cancer.