Additionally, it is considered that stressed keratinocytes are responsible for the production and release of CXCL10 to recruit lymphocytes into the epidermis and promote the melanocytotoxic activity of CD8+; in comparison, the inhibition of CXCR3 by antibodies decreases the presence of CD8+ lymphocytes in lesions in animal vitiligo models [20,21,22]. This evidence concerns the gene CXCL10 and vitiligo.