Before attempting to target this gene to the germline of mice, this construct or a 5′ deletion construct with truncated 5′ regulatory regions lacking the [ATAAA]n pentad repeat (Fig. 1A), was transfected into Hep3B human liver cancer cells, which are normally devoid of π-class GSTs as a result of epigenetic silencing of hGSTP1 attributable to somatic CpG island hypermethylation [16]. This evidence concerns the gene HPGDS and liver cancer.