The ZEB1 promoter responding such signals converted from a bivalent to active chromatin configuration to increase ZEB1 transcription and then non‐CSCs subsequently entered the CSC state.37 In some reports, HIF‐1α promoted ZEB1 expression and EMT in hypoxia and this HIF‐1α/ZEB1 axis contributed the enhancement of cancer cell aggressiveness in such migration and invasion or distant metastasis in bladder cancer and glioblastoma.38, 39 In our study, HIF‐1α and ZEB1 were both significantly and relatively upregulated in AC than in AB by the DNA microarray analysis. This evidence concerns the gene HIF1A and cancer.