In fact, because fibroblasts with defective p53 undergo senescence at much lower rates than NFs, there is a selection for mutant p53- or p53-deficient fibroblasts that promote tumor progression in the TME in vivo [237], suggesting that tumor progression may involve a process of non-mutational modification of p53, switching its effects from tumor-suppressive to tumor-enhancing transcriptional programs [235]. Here, TP53 is linked to neoplasm.