We read with interest and appreciate the paper by Fujii et al., 1 but feel it is necessary to make the following observations. Despite advances in our cellular and molecular knowledge, hepatocellular carcinoma (HCC) remains one of the major public health problems throughout the world. It is now known to be highly heterogeneous as it encompasses various pathological entities and a wide range of clinical behaviors, and is underpinned by a complex array of gene alterations that affect supra-molecular processes. 2 Pituitary tumour transforming gene 1 (PTTG-1) is an oncogene expressed in various human neoplasms and cell lines. [3][4][5][6][7][8] Although its pathogenetic implications in HCC are still unknown, it has been shown that its over-expression in hepatoma cell lines negatively regulates the ability of p53 to induce apoptosis, and that its silencing by means of short interference RNA may be an efficient way of treating liver cancer. 8 The expression of tumor-associated antigens is mainly investigated at the gene level by means of quantitative real-time PCR (qrt-PCR). However, the information provided by this approach is limited by the fact that the phenomena observed at each level of anatomical organization (i.e., genes, sub-cellular entities, cells, tissues, organs, apparatuses and organisms) have properties that do not exist at lower or higher levels: qrt-PCR offers an adequate quantitative description of small-scale structures, but this is likely to be inapplicable when it comes to large-scale features. 9 We used an immunoperoxidase-based staining assay to investigate the expression of PTTG-1 (anti-PTTG-1 polyclonal antibodies,