Thus, collectively our data from chronically treated animals, acute treatments of the isolated mesenteric vascular bed, and from cultured VSMC grown in high glucose, provide strong evidence that activation of ErbB2, heterodimer formation with EGFR, and downstream signaling via ERK1/2-ROCKs as an important pathway mediating vascular dysfunction associated with diabetes (see our working model in Figure 11). The gene discussed is EGFR; the disease is diabetes mellitus.