The modeling results showed that persistently inhibiting phosphatidylinositol 3-kinase (PI3K)/Akt activity induce the switch of GC cell attractors to cell-cycle-arrest and apoptosis-like attractor (Supplementary Figure 6), indicating that PI3K/Akt is a critical component of cancer-related PFLs and persistently inhibiting the PI3K/Akt signaling pathway may increase the susceptibility of cancer cells to apoptosis. Here, AKT1 is linked to cancer.