Akt activity increases in response to TGFβ treatment, which seems to be required for a variety of TGFβ-induced activities, such as cell migration of HER2-expressing breast cancer cells, EMT of normal mammary epithelial cells, cell survival of mouse hippocampal neurons and mesenchymal cells, as well as growth stimulation of certain fibroblasts (74, 75). The gene discussed is AKT1; the disease is breast carcinoma.