A cross-talk between AngII and EGFR has been shown to play a pivotal role in stimulating the development of renal lesions [19]; chronic infusion of AngII in mice resulted in glomerulosclerosis and interstitial fibrosis, while transgenic mice for a dominant negative isoform of EGFR or TGF-β−/− mice were protected from these lesions. The gene discussed is EGFR; the disease is glomerulosclerosis.