TP53 and renal fibrosis: In addition, the myofibroblasts show increased expressionof p53 and Ki67. During renal fibrosis,TGFβ1activates reactive oxygen species-dependent pathways, thereby inducinggene expression of p53 and EGFR.47,48 The former,as a coactivator of TGFβ1, controls apoptosis, cell growth,and stress responses and promotes fibrosis.48,49 Targeting p53 gene expression is a valid strategyto mitigate fibrosis.49 Easy detectionof (increased) p53 expression in the small scalesamples is very attractive in developing drugs against fibrosis andother diseases, including cancer.