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Autoimmunity, melanocyte adhesion, and metabolic dysfunction have been suggested as contributing to the etiology of vitiligo, and several genes based on the above mechanisms have been tested.31 Noteworthy examples include the DDR1 gene, which encodes a transmembrane tyrosine kinase receptor that is the main adhesion protein of melanocytes to the basement membrane and has been shown to be downregulated in vitiligo in comparison to unaffected skin.32,33 DDR1 forms a complex with E-cadherin (encoded by CDH1), which is important for the maintenance of the epithelial structure