Since GRHL3 is highly expressed in human chronic wounds (Figure 1), we next investigated whether components of the GRHL3/FSCN1/E-cadherin pathway are altered in mouse diabetic wounds, a model of delayed wound healing where mice are made diabetic through high-fat feeding (27) (Figure 6D; n = 3); diabetes was confirmed with fasting glucose measurements (fasting blood glucose > 200 mg/dL). This evidence concerns the gene FSCN1 and diabetes mellitus.