Interestingly, these abilities are also transmissible to non-transformed cells: by promoting secretion of podocalyxin-rich exosomes, mut-p53 R273H and R175H proteins were found to modulate RCP/DGKα-dependent endosomal recycling in receiving normal fibroblasts that populate the TME of primary and secondary tumor sites, inducing their α5β1 integrin-dependent activation to a cancer associated (CAF) phenotype, increasing tumor invasiveness (64). Here, TP53 is linked to cancer.