Thus, identification of therapeutics that bias the IGF-1R to selectively activate Akt would address potential concerns that IGF-1 may exacerbate microvascular dysfunction in diabetes through ERK, as it can also play a role in VEGF-induced RNV [43] since IGF-1-induced VEGF expression is ERK-dependent [44]. The gene discussed is AKT1; the disease is diabetes mellitus.