Figure 3F (Supplementary Figure S9) shows the levels of GPC3 in six fresh HBL specimens. In some HBL patients, we observed two GPC3 isoforms with MW 70 kD and 90 kD, suggesting the possibility of post-translational modifications of GPC3 in HBL patients (Supplementary Figure S2). Taken together, the activation of the β-catenin-TCF4 pathway in aggressive HBL leads to the opening of CEGRs/ALCDs in GPC3 and to the increased expression of GPC3. The gene discussed is TCF4; the disease is hepatoblastoma.