In this study, we clarified that the mechanism of TRAIL-resistance consisted of not only a decrease in the expression level of DR5 and also malfunction of its recruitment to the cell surface, as evidenced form the results obtained by using TRAIL-resistant human colon cancer DLD-1 cells and human mammary gland epithelial MCF10A cells and their cancer stem-like cells (Fig. 1C). This evidence concerns the gene TNFSF10 and colonic neoplasm.