clear association with any particular G-6-PD variant was discernible.All G-6-PD-deficient homozygotes also carried G-6-PD Viangchan vari-ant. According to WHO classification, only G-6-PD Chinese-5 is classifiedas class III type (mild deficiency, 10–60% residual enzymatic activity),whereas G-6-PD Viangchan, Canton, Union and Kaiping are classifiedas class II (severe deficiency, b10% residual enzymatic activity) [28].These data support the study of Filosa et al. [29] that somatic cell selec-tion plays a major determining role on the phenotype of G-6-PD-deficient heterozygotes. Moreover, as severe G-6-PD deficiency ad-versely affects the proliferation or survival of pluripotent hematopoieticstem cells, this phenotypic characteristic is critical during hematopoie-sis. Recent report indicates that specific CpG hypermethylation withinthe G-6-PD promoter and preferential X chromosome inactivation ofthe wild-type allele are major determinants of the phenotypic varia- tions in female G-6-PD-deficient heterozygotes [30]. Thus, biochemicalassay of G-6-PD activity is not a reliable method to identify heterozy-gotes and G-6-PD mutation analysis will be a more appropriate ap-proach