Upon ligand binding, IGF-1R becomes auto-phosphorylated and subsequently recruits specific docking intermediates, including insulin-receptor substrate-2 (IRS-2), that activate PI3K/AKT and Ras/Raf/MAPK pathways in order to promote cell motility and pro-metastatic behaviour in breast cancer cells [129,132,133] (Figure 2D). This evidence concerns the gene AKT1 and breast carcinoma.