Considering such similarities between hMSCs and CAFs and strong evidences showing transition of hMSCs into CAFs in tumor microenvironment, we speculate that the initial cancer cell death induced by chemotherapy or radiation may cause a feed-forward stimulation in the CAFs and thereby the CAFs can suppress tumor progression or metastasis by upregulating expression levels of TRAIL and IFN-β in TRAIL-sensitive breast cancer patients. This evidence concerns the gene IFNB1 and neoplasm.