This finding is important because signaling via HER2 alone or with its dimerization partners HER1 or HER3 represents a well-established endocrine resistance mechanism based on experimental studies of HR + breast cancer cell lines25, in vivo tumor studies26, and most importantly by frequent HER2-upregulation in recurrent metastases after anti-estrogen therapy10,27–30. This evidence concerns the gene ERBB3 and breast carcinoma.