Their results were similar to the previously described: (i) the concordance between HER2 amplification and HER2-E subtype was really poorly (only 47% of HER2 amplify tumors presented this intrinsic subtype); (ii) it was find no evidence for cooperating copy number drivers with HER2 outside chromosome 17, and finally (iii) after the transcriptional profiling of the HER2-E subtype, the authors reported that HER2+ tumors are hormonally driven, either by ER in hormone receptor-positive and HER2-E BC, or by AR in hormone receptor-negative and HER2-E BC (93). This evidence concerns the gene ESR1 and breast cancer.