More recently, the weight of evidence has supported a role for ErbB3, rather than ErbB4, with increased activation of ErbB3 being reported in acquired tamoxifen- and fulvestrant-resistant MCF-7 cells [27,28] and its downregulation-enhancing responsiveness of ErbB2-overexpressing, de novo antihormone-resistant breast cancer cells to tamoxifen [29]. This evidence concerns the gene ERBB2 and breast carcinoma.