ATL-1 from AMK  • Inhibited cell viability and induced apoptosis• Inactivated Notch signaling (Notch1, Jagged1, Hes1, and Hey1)• Reduced the self-renewal and colony formation abilities of GCSLCs• Decreased the expression of CD44• ATL-1 can potentially inhibit cancer cell proliferation and induce apoptosis through inactivating Notch pathway. Here, HES1 is linked to cancer.