GLI1 and acute myeloid leukemia: These data indicated that inhibition of EZH2 either pharmacologically by chidamide or genetically by shEZH2 decreased the activity of Smo/Gli-1 pathway and increased adriamycin sensitivity, and genetic EZH2 overexpression reduced the cytotoxicity of chidamide and restored the resistance to adriamycin in AML cells.