Instead, we found that phosphorylated AKT, β-catenin, and GSK3β levels were slightly down-regulated by the combinatorial drug treatment in both cell lines (Figure 3C,D), suggesting that the PI3K/Akt and Wnt/β-catenin pathways may be involved in targeted oncogene addiction selectively for the RAS-mutant colon cancer cells. Here, AKT1 is linked to malignant colon neoplasm.