GLI1 is an indicator for activating the hedgehog pathway associated with drug resistance in AML, as well as the survival and expansion of BCR-ABL-positive leukemic stem cell.[61,62] GLI1 overexpression caused an increase in the phosphorylation of PI3K and AKT and upregulation of cell cycle regulators GSK3α/β, cyclins D (cyclin D2 and D3), CDK4, and CDK6 that resulted in hyperproliferation and drug resistance in AML.[44] The increase in CDK4 and CDK6 expressions guided the rationale for treating the cells with a combination of the GLI1 inhibitor, GANT61, and the CDK6 inhibitor, palbociclib. Here, GSK3A is linked to acute myeloid leukemia.