Cellular response to etoposide when TOP1 was suppressed by miR-23a may be indicated by the increasing impaired cell progression through S phase upon etoposide treatment (Figure 2D), and interestingly, cell cycle progression of wild-type and miR-23a-overexpressed HCC cells with treatment of 5-Fu have no differences (Additional file 1: Figure S2) These data suggest that simultaneous down-regulation of TOP1-mediated enhanced response to etoposide may be responsible for the enhancing sensitivity to TOP2A poison in HCC cells with miR-23a overexpression. The gene discussed is TOP1; the disease is hepatocellular carcinoma.