Although our data does not rule out the possibility of ErbB2 heterodimerization with other family members, the fact that both diabetes-induced elevation in ROCK and ERK1/2 activity in the mesenteric vascular bed was also markedly corrected by chronic or acute EGFR inhibition (Figures 5) further supported our notion that ErbB2/EGFR heterodimerization with subsequent activation of ROCK and ERK1/2 led to diabetes-induced vascular dysfunction. Here, ERBB2 is linked to diabetes mellitus.