CCL5 and neoplasm: In addition, a tumor–MSC–tumor feedback loop involving CCL5 signaling (Karnoub et al., 2007) and enhanced collagen deposition via discoidin domain receptor (DDR)-2 on TA-MSCs (Gonzalez et al., 2017) has been shown to stimulate breast cancer motility, invasion, and fibronectin alignment (Erdogan et al., 2017); enhance TA-MSC engulfment by breast cancer cells linked to enhanced metastatic potential (Chen et al., 2019); and enhance TA-MSC-derived exosomes by cancer stem cell thus boosting glioma aggressiveness (Figueroa et al., 2017).