Our results displayed that the expressions of SIX1, Cyclin D1, and Ki-67 (a well-accepted proliferation marker) in tissues were notably reduced by the administration of SNS-032, while the expression of c-Caspase 3 (the activated form of Caspase 3) was increased in the treated group (Fig. 5E-F), indicating that SNS-032 can also trigger SIX1 downregulation, cell cycle arrest, and apoptosis in HCC xenografts established on mice models. Here, SIX1 is linked to hepatocellular carcinoma.