In recent years, extensive genome‐wide associated studies shed light on more than 40 susceptibility loci, including MC1R, TYR, IFIH1, CD44, CD80, GZMB, HLA‐A, XBP1, CAT, and MTHFR. 7, 8Of the identified candidate loci, more than half are involved in immunoregulation, T‐cell receptor repertoire, and immune cell‐associated apoptosis, indicating the critical effect of aberrant immune function in vitiligo pathogenesis.8 The gene discussed is HLA-A; the disease is vitiligo.