FasL has been shown to be important in the protection of tissue grafts from rejection. The aim of this study was to determine whether transfection of FasL into human heart valve endothelial cells can hinder immune rejection by induction of apoptosis in T cells. Human FasL cDNA was cloned into a mammalian expression vector containing the neomycin resistance marker. The endothelial cell line HMEC-1 was transfected with the plasmid and selected with antibiotic. Cultures from positive clones were analyzed by semi-quantitative PCR, RT-PCR and Western blot to determine the FasL transfection and expression. Cytotoxic assays were subsequently performed to detect the FasL function in those transfected cells. High copy number transfected cell lines were produced, and mRNA and protein expression were confirmed. Preliminary results from cytotoxic assays show that transfected cells have enhanced cytotoxicity in comparison with their parent cell line.