In summary, we found that (1) HER2 was neither amplified nor overexpressed in both HCC tumor tissues and nontumor tissues; (2) TOP2A overexpression in HCC tumor tissues did not arise from TOP2A gene amplification and was independent from HER2 gene amplification or overexpression; and (3) TOP2A overexpression was significantly associated with HBsAg in the serum, as well as with Ki-67 expression. This evidence concerns the gene MKI67 and neoplasm.