We recently discovered that the erbB2 receptor simultaneously interacted with erbB3 and IGF-1R to form a trimeric complex in trastuzumab-resistant breast cancer cells, and that it was the hetero-trimerization of erbB2/erbB3/IGF-1R, not the hetero-dimer of erbB2/erbB3 or IGF-1R/erbB2, that played a critical role in the breast cancer cells resistant to trastuzumab [75]. The gene discussed is IGF1R; the disease is breast cancer.