While our research group [52] showed that the genetic deletion of receptor Mas in C57Bl/6 mice led to glomerular hyperfiltration, proteinuria and renal fibrosis, Esteban et al. [28] reported that renal deficiency of Mas diminished renal damage in unilateral ureteral obstruction and in ischemia/reperfusion injury, and that the infusion of Ang-(1-7) to wild-type mice elicited an inflammatory response. This evidence concerns the gene MAS1 and renal fibrosis.