The metabolic activities of major isoforms in UGT1A, UGT1A1, UGT1A9, UGT1A4 and UGT2B7 in HBV-positive HCC tumor human liver microsomes (HLMs) and the adjacent normal HLMs were investigated, respectively, by utilizing the specific substrate of each UGT such as SN-38 [11,22,23], propofol [24], genistein [25], tamoxifen and zidovudine. This evidence concerns the gene UGT2B7 and neoplasm.