A typical foot ulcer in a person with diabetes is shown at top. (i) The nonhealing edge (callus) containing ulcerogenic cells with molecular markers indicative of healing impairment. (ii) Phenotypically normal but physiologically impaired cells, which can be stimulated to heal. Despite a wound’s appearance after debridement, it may not be healing and may need to be evaluated for the presence of molecular markers of inhibition and/or hyperkeratotic tissue (e.g., c-myc and β-catenin). We expect more such molecular markers will be identified in the future. Once a wound is debrided, pathology analyses along with immunohistochemistry should determine whether the extent of debridement was sufficient. If the extent of debridement was not sufficient (lower left diagram), cells positive for c-myc (green) and nuclear β-catenin (purple) will be found, indicating the presence of ulcerogenic cells, which will prevent the wound from healing and indicate that additional debridement is necessary. Lack of healing is also demarcated by a thicker epidermis, thicker cornified layer, and presence of nuclei in the cornified layer. If the debridement was successful (lower right lower diagram), no staining for c-myc or β-catenin will be found, indicating an absence of ulcerogenic cells and successful debridement. These markers of inhibition are useful, but the most important goal is actual healing as defined by the appearance of new epithelium, decreased area of the wound, and no drainage. This information should be stored electronically in the Wound Electronic Medical Record (WEMR), which provides an objective analysis coupled with pathology and microbiology reports.