Objective: To investigate whether FasL expression by exogenous FasL gene transfer had regulatory effect on drug sensitivity of tumor cells. Methods: Exogenous Fasl, gene transfer was mediated by lipofectAMINE. The FasL expression was detected bv Immunohistochemistry and RT-PCR. The growth inhibition of cytotoxic drugs on tumor cells was measured by MTT assay. Fas mRNA expression was analyzed bv Semi-quantitative RT-PCR. Results: The eukaryotic expression vector, PcDNA3-FasL and PcDNA3 were successfully transteeted into MCF-7 cells. The transfectant cells was named as MCF-7/FL or MCF-7/Vt respectively. FasL was expressed on MCF-7/FL but not on MCF-7/Vt or MCF-7. The cytolysis ot MCF-7/FL induced by adriamycin at concentration of 0.625 ~ 2.5 ?g/ml, cisplatin of 1 .25 ~ 10 ?g/ml, or methotrexate of 3 ~ 6 ?g/ml respectively were all significantly enhanced compared with the cytolysis of MCF-7. Blocking FasL by using F(ab' )2-anti APO-1 antibody markedly reduced this up-regulated cytolysis induced by these drugs The significant up-regulation of Fas mRNA on MCF-7/FL was observed by Semi-quantitative RT-PCR after these drugs treatment. Conclusion: These findings indicated that FasL expression by gene transfer had up-regulation effect on drug sensitivity of tumor cells, this effect was associated with enhanced Fas expression induced by cytotoxic drugs.