Melanocytes are specialized neural crest-derived cells that are responsible for skin pigmentation. In vitiligo, loss of functioning epidermal melanocytes results in loss of pigment. Based on published studies, many transcription factors including microphtalmia-associated transcription factor, SRY (Sex Determining Region Y)-Box 10 are responsible for differentiation of melanocytes from neural crest cells as well as development of melanoblasts). However, the pathogenesis of loss of pigmentation in skin still unclear. We studied the expression of several melanocyte-related proteins and markers in vitiligo samples and comparing them to normally pigmented skin samples. This may provide a more insight into the pathogenesis of vitiligo which is a still controversy. We assessed the expression of six antibodies including S100, Melan-A (to detect fully formed, functioning melanocytes), CD117 (a specific relevant tyrosinase inducer), MITF and SOX-10 (important related transcription factors), and BCL-2 (stem cell markers) in 32 skin samples. We demonstrated significant decline in the expression of all examined immunomarkers in the skin of vitiligo when compared to normal pigmented skin. Our data may speculate that vitiligo pathogenesis does not involve only destruction of functioning active melanocytes, but also, other steps of cellular stimulation of induction of melanocytes and melanogensis are significantly affected as well.