In preclinical models of HR-positive breast cancer, the recurrent HER2 L755S and V777L mutations constitutively upregulated HER3 phosphorylation, particularly upon treatment with fulvestrant, resulting in hyperactivation of the HER3/PI3K/AKT/mTOR signaling axis and leading to antiestrogen resistance[12,22]. This evidence concerns the gene ERBB3 and breast carcinoma.