At a dose and treatment regimen previously shown to correct diabetes-induced vascular dysfunction, we firstly showed that chronic in vivo or acute (ex vivo) Ang-(1–7) treatment can inhibit diabetes-induced transactivation of ErbB2 receptor at multiple tyrosine sites (namely Y1221/1222, Y1248 and Y877) and correct changes in downstream signaling molecules (ERK1/2, p-38 MAPK, ROCK2, eNOS and IkB-α) within the mesenteric vascular bed without correcting the underlying hyperglycemia. This evidence concerns the gene MAPK3 and Hyperglycemia.