identified fibroblast growth factor receptor 4 (FGFR4) as a necessary gene for HER2-positive breast cancer to acquire resistance; inhibiting FGFR4 in mice can reduce GSH synthesis and efflux efficiency of Fe2+ through the β-catenin/TCF4-SLC7A11/FPN1 axis, leading to excessive ROS production, LIP iron accumulation, and ferroptosis, enhancing the sensitivity of drug-resistant HER2-positive breast cancer to chemotherapy drugs (106). This evidence concerns the gene SLC40A1 and breast carcinoma.