In the context of Th17 inhibition, the Th1 immune response may be relatively active due to lack of regulation (83), thereby enhancing the activation of the IFN-γ/CXCL10 axis, promoting CXCR3+ CD8+ T cell recruitment and melanocyte destruction, and inducing or aggravating vitiligo. This evidence concerns the gene CXCR3 and vitiligo.