Other investigators reported the increased binding of PSA from sera of patients with prostate cancer but not with BPH to TJA-II (Trichosanthes japonica agglutinin-II), which interacts with glycans terminated with the GalNAcβ1 →  group in addition to those with the α-1,2-linked fucose residue [34], suggesting that the expression level of the LacdiNAc group on the PSA glycans increases in human prostate cancer.The ratios of TJA-II-bound PSA to total PSA in sera of prostate cancer patients and in those of BPH patients were reported to be 8.3 ± 5.6% and 1.0 ± 0.55%, respectively [21]. This evidence concerns the gene KLK3 and Familial prostate cancer.