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. This evidence concerns the gene EGFR and renal fibrosis.