The development of such agents is based on the rationale provided by studies showing that knocking out of TRAIL or blockage of TRAIL-receptors leads to enhanced tumor and metastasis formation in vivo[6] and that loss of TRAIL-receptors expression in human cancer tissues correlates with poor prognosis and tumor recurrence (Reviewed by Walczak and colleagues [7]). This evidence concerns the gene TNFSF10 and neoplasm.