AKT1 and neoplasm: To test this possibility, we performed an oral glucose tolerance test in MC38 tumor-bearing mice and observed a transient postprandial increase in phosphorylation of Akt in tumor (pSer473), which was slightly delayed as compared to plasma insulin concentrations, and an increase in tumor pThr389 p70 S6K (Fig. 7a, b, Additional file 1: Figure S5A-B), demonstrating that tumor insulin signaling indeed is acutely altered in response to normal physiological changes in insulin concentrations.