This could be explained by either one of the following factors: (i) the overexpression of DSG2 by tumor cells, (ii) better accessibility of DSG2 on tumor cells due to a lack of strict cell polarization compared to DSG2-expressing normal epithelial cells, or (iii) a high degree of vascularization and vascular permeability in tumors. The gene discussed is DSG2; the disease is neoplasm.