Because m6A-hypomethylation regulated FGFR4 phosphorylates GSK-3β and activates β-catenin/TCF4 signaling to drive anti-HER2 resistance, FGFR4 inhibition enhances susceptibility to anti-HER2 therapy in resistant breast cancer by reducing glutathione synthesis and Fe2+ efflux efficiency via the β-catenin/TCF4-SLC7A11/FPN1 axis and labile iron pool accumulation (Zou et al., 2022). This evidence concerns the gene ERBB2 and breast carcinoma.