In order to dissociate the contributions of GH and IGF-1-excess from the development of kidney damage, Blutke et al. compared the renal phenotype of IGF-1-deficient mice (I-/-), IGF-1-deficient GH-transgenic mice (I-/- /G), GH-transgenic mice (G), and wild-type mice [122, 123]. This evidence concerns the gene GH1 and Nephropathy.