Half of the HER2+ breast cancer patients are initially nonresponsive or acquire resistance to anti‐HER2 therapy,2, 3 and oncogenic mutations of PIK3CA play a vital role in constitutively activating the phosphoinositide 3‐kinase (PI3K)/protein kinase B (AKT)/mechanistic target of rapamycin (mTOR) downstream signalling pathway.4 This evidence concerns the gene MTOR and breast cancer.