To model molecular interactions in sufficient complexity, we used ModCellTM [11–13], a mechanistic model based on cancer-related signaling pathways such as the Hedgehog, Wnt, RAS/MAPK, and PI3K/AKT/MTOR signaling, that either enhance MYC transcriptional activity or suppress apoptosis via effector caspases (Fig. 1F). Here, AKT1 is linked to cancer.