To define chemotactic signals that could mediate aberrant recruitment of leukocytes to RDEB skin wounds [4], we analyzed 13 most common wound-bed-associated pro-inflammatory chemokines (CCL2, CCL3, CCL4, CCL5, CCL11, CCL17, CCL20, CXCL1, CXCL5, CXCL8, CXCL9, CXCL10, CXCL11) in wound exudates. This evidence concerns the gene CCL2 and recessive dystrophic epidermolysis bullosa.