Upon ligand binding, IGF-IR becomes autophosphorylated at Tyr 1131, 1135, and 1136 in the β subunit and subsequently recruits a host of proteins, including IRS-2, that activate signaling via PI3K/AKT and Ras/Raf/MAPK pathways to promote cell motility and pro-metastatic behavior in breast cancer cells [10,15,16]. This evidence concerns the gene IGF1R and breast cancer.