Interestingly, a recent study showed that a subset of EGF-deficient mice developed crescentic glomerulonephritis due to upregulated HB-EGF/EGFR activation in glomeruli (Zeid et al., 2022) implying also that physiological levels of EGF, as well as HB-EGF, act as reno-protective agents against the development of glomerulonephritis. This evidence concerns the gene EGF and glomerulonephritis.