Additionally, the insulin–TOR–MAPK network model developed by Nijout and Callier [141], which correctly demonstrated that MAPK, active PI3K and GLUT4 responded in a dose-dependent manner to insulin, demonstrated that at lower insulin levels, PTEN knockout increased protein synthesis, and increased insulin sensitivity by GLUT4 activation, consistent with PTENs role as a tumour suppressor. Here, SLC2A4 is linked to neoplasm.