Introduction - Vitiligo is the most frequent acquired hypomelanosis, but it's etiology is still uncertain. Many patients conect the onset to physical trauma, stress or illness. Nowadays new thoeries have been undertaken. It is clear that several different processes are involved in the etiology of vitiligo. Aims & Scope - to analyse possible conections between the onset of vitiligo with other associated diseases, that have occurred in our patient’s life. The aim is also to mention about the new theory of the pathogenesis of vitiligo. There are some myths about the vitiligo, because of the misconnection of the vitiligo lesions and that occurs in for example leprosy or in sexually transmitted diseases. That myths have made the vitiligo a stigma in many societies.That problem has also been mention in the presentation. Results - there have been revealed that the onset of vitiligo in this patient may be conected with the prevalence of others autoimmune disorders like thyroid disease, diabetes mellitus, alopecia areata. There was also family history of vitiligo – three patient’s daughters suffered from late onset vitiligo. Additionally there was a significant stress related trigger factor in patient’ life, that could have the influence on the onset of the disease. Comments – Vitiligo is a disorder with a genetic background. The genes of susceptibility to the vitiligo are also connected with other autoimmune disorders. The environmental triggering factors play also a significant role in the onset of the vitiligo. Both melanocytes and nerves arise from a neural crest cells, and this is a basis of the neurohumoral hypothesis of the etiology of vitiligo. Oxidative stress hypothesis is based on a fact that this process may lead to melanocyte destructions and there are high H2O2 levels throughout the epidermidis in patients with vitiligo. The melanocytorragy hypothesis may be the explenation for the Koebner phenomenon in vitiligo. The decreased melanocyte survival hypothesis is associated with the decreased number of tyrosine kinase receptor c-kit in perilesional melanocytes, and with the lower expression of stem cell factor from surrounding keratinocytes. That may lead to vitiligo onset, causing the deficiency in survival signals leading to the melanocyte apoptosis. Questions – 1. Is the Koebner phenomenon connected with the: - Oxidative stress hypothesis - Decreased melanocyte survival hypothesis - Melanocytorragy hypothesis ? 2. What play the significant role in the oxidative stress hypothesis : - Elevated levels of tenascin in the vitiligonous skin - Decreased number of tyrosine kinase receptor c-kit in perilesional melanocytes - Low levels of catalase enzyme in the skin of vitiligo patients ? - Disclaimer- This PPT is loaded as student material "as is", from the Vitiligo Master Class Barcelona November 2011; VRF does not endorse or otherwise approve it.