Various mechanisms have been reported to cause resistance of breast cancers to trastuzumab, including reduced HER2 expression or antibody affinity, increased pro-survival signaling through alternative receptor tyrosine kinases, and altered intracellular signaling such as the loss of PTEN expression, reduced activity of cell cycle regulator p27kip1, or increased Akt activity, which result in the over-proliferation of cells[8,9]. This evidence concerns the gene ERBB2 and breast cancer.