In this model, the tumor growth process is replaced with the cell cycle model from figure 7. Components of the hedgehog pathway now interact directly with cyclin D1; mitotic cyclin (cyclin B) is required for Nmyc phosphorylation to the active Nmyc-P state. b. If the cell cycle is activated by injecting Nmyc-P initially, the effect of other components on the cycle can be studied. In this figure, IGF is decreased beginning on day 6, allowing GSK-3β to increase. Nmyc-P is then phosphorylated and degraded. The effects of drug dose will be the same for this model as in figure 9, as the primary action of the drug on Gli2 has not been changed. However, adding details to the cell cycle now allows more detailed investigation of the interaction between the drug, its targets, and cell cycle components.