Since, β-catenin activation in HCC can be due to multiple independent mechanisms such as overexpression of Wnt inhibitors, increased expression of Wnt3 and Frizzled-7, TGF-β activation or other reasons [2], [7], [8], [17], [22], [27], [28], we also examined if serum LECT2 may in fact reflect β-catenin activity rather than its mutational status. The gene discussed is TGFB1; the disease is hepatocellular carcinoma.