Together with our previous findings, HER2-mediated MED1 activation through MAPK signaling and our current findings on the miR-205 regulation of both HER3/PI3k/Akt and MED1 suggest a complex molecular interaction and crosstalk between the HER2, HER3, PI3K-AKT, MAPK signaling axes, where MED1 and miR-205 could play crucial roles in regulating the treatment resistance of breast cancer. The gene discussed is MED1; the disease is breast cancer.