The focus on TRAIL as a potential therapeutic agent became obvious owing to its differential sensitivity to observe between normal and cancerous cells (Ashkenazi et al, 1999; Walczak et al, 1999), while its major advantage lies with its ability to trigger tumour cell apoptosis in a variety of cancers independent of p53 status (Pitti et al, 1996; Galligan et al, 2005). This evidence concerns the gene TNFSF10 and neoplasm.