In summary, the data presented in this study demonstrate dissociated effects of GH and IGF1 in excess GH‐stimulated tubular and glomerular growth in vivo, and indicate that (1) IGF1 is not necessary for mediation of the effects of GH‐overabundance causing progressive glomerulosclerosis in GH‐transgenic mice; and (2) IGF1 is an important mediator of excess GH‐induced proximal tubular hyperplasia. The gene discussed is GH1; the disease is glomerulosclerosis.