Epithelial–mesenchymal transition is a possible mechanistic basis for anti-cancer drug resistance.17 To the best of our knowledge, the SIX1-dependent effects on drug treatment have only been investigated in gastric and breast cancer cells.8,18 To further determine the effect of SIX1 in HCC, shSIX1 and control cell clones were treated with sorafenib, which is a standard chemotherapeutic drug for HCC. This evidence concerns the gene SIX1 and breast carcinoma.