We investigated the therapeutic implications of CD36 inhibition in HER2 + BC and found that dual CD36 and HER2 blockade significantly enhanced the therapeutic benefit of HER2 blockade both in vitro and in vivo by targeting HER2 +/CD36 + EMT-like stem-like cells in lapatinib-refractory cell models and by reducing tumor growth in mice implanted with CD36-silenced MDAMB361 cells compared with mice implanted with control cells. This evidence concerns the gene CD36 and breast cancer.