Our results indicate that (1) Ang‐II‐induced renal fibrosis not only developed more slowly than cardiac fibrosis, but was also mediated by TNFR1‐dependent mechanisms involving uptake of myeloid fibroblast precursors, and (2) TNFR1‐KO mice remained protected from the development of cardiac and renal fibrosis despite a delayed increase in systolic blood pressure and decrease in cardiorenal function. This evidence concerns the gene AGT and renal fibrosis.