In a gastric cancer precancerous model, p53 deficient bone marrow-MSCs could secrete UBR2-rich exosomes, which activate the Wnt/catenin pathway in tumor cells and result in tumor growth, motility, and stemness (87). MSC exosomes could also induce chemoresistance in gastric cancer cells by antagonizing 5-fluorouracil-induced apoptosis and enhancing expression of multidrug resistance-associated proteins (88). Here, TP53 is linked to neoplasm.