These studies suggest that mTORC2 coordinates two signaling pathways, Akt and PKCα, which destabilize the Rac inhibitor RhoGDI2, while using Akt to activate the Rac-GEF Tiam-1, to achieve maximal Rac activation and cell motility, supporting metastasis in HER2-amplified breast cancers (Fig. 6g). This evidence concerns the gene ARHGDIB and breast cancer.