In this scenario, hr-IGF1/IGFPB-3 could act by minimizing the endothelial dysfunction and renal tubular damage as described in previous rodent models of AKI.1,2 However, an specific role of IGF-1 in renal glomerular angiogenesis or preventing glomerular neonatal hemorrhages has not been described before, and more studies are needed to determine whether IGF-1 can indeed play such a role, and if so, what is the mechanism. The gene discussed is IGF1; the disease is endothelial dysfunction.