It can also induce drug resistance by modulating drug metabolism as GLI1 induces the expression of UDP glucuronosyltransferase (UGT1A), which inactivates drugs by glucuronidation in chemotherapy-resistant AML cells, and the inhibition of GLI1 activity either through siRNA-mediated knockdown or treatment with the SMO inhibitor vismodegib sensitizes AML cells to cytarabine or the eIF4E inhibitor ribavirin [34]. This evidence concerns the gene GLI1 and acute myeloid leukemia.