Colorectal cancer cells also have a high level of activity of HedgeHog (HH)-GLI signaling, and the self-renewal of CCICs relies on the direct function of HH-GLI activity in xenograft tumors [12]; Akt can activate 14-3-3zeta in the beta-catenin complex, which contributes to the stabilization and nuclear translocation of β-catenin, thus facilitating CCSC self-renewal by activating Wnt [13]. This evidence concerns the gene GLI1 and colorectal cancer.