There are several arguments suggesting that vitiligo is a genetically dependent disease. Certain animals have comparable pigment disturbances (Smyth chickens, C57BL/6J-mi(vit)/mi(vit) mice and B light mice). Genetic studies have demonstrated that certain genes are crucial for the development of vitiligo. Familial cases and cases reported in twins are further arguments. There is a high risk for both children and siblings of a subject with vitiligo. Several HLA studies have been reported. Most show sporadic association between vitiligo and certain HLA groups, but there is no clear and regular association with any of the class I or II alleles. Intrinsic melanocyte anomalies which persist in cell culture also favour the genetic theory. Vitiligo is probably a polygenetic disease, simultaneous alterations in several genes either causing he disease or increasing susceptibility. One speculation would be that one or more genes are responsible for premature death of melanocytes. Likewise, genes affecting melanocyte growth either directly or via paracrine factors (genes coding for the keratinocyte melanotrophic factor, for example), and the combined effects of genes controlling autoimmune phenomena could be involved. Despite formal proof that vitiligo is genetically dependent, and despite rapid progress in molecular genetics, the gene or genes directly implicated in this dermatosis remain to be identified.