Consistently it was observed in our study that TOP1 down-regulation by miR-23a in HCC cells could largely potentiate cells to etoposide and doxorubicin treatment but not 5-Fu exposure, and forced overexpression of miR-23a in HCC cells reduced the cytotoxicity of TOP1 poison irinotecan, whose activity was dominated by the content of endogenous TOP1 level [8]. The gene discussed is TOP1; the disease is hepatocellular carcinoma.