Atopic dermatitis is chronic inflammatory disease characterized by severe itch and typical clinical picture. Besides genetic there are other factors such as the environmental influence, damaged barrier function and various other. Multiple studies have shown that vitamin D has influence on activation of signals that leads to synthesis of cytokine responsible for causing allergic inflammation that reminds on atopic dermatitis. The aim of this experiment was to prove atopic dermatitis induced with topical application of analogue of vitamin D (MC903) in mouse. Experimental group we treated with analogue of vitamin D (MC903) mixed with ethanol while the control group was treated with ethanol. All mice from experimental group developed characteristic AD-like phenotype. Weight of ears mice from experimental group was significantly higher compared to weight of ears mice from control group. Histologic analysis of ears mice from experimental group revealed epidermal hyperplasia and a heavy dermal cell infiltrate. In second experiment one randomly selected mouse from both groups was sacrified every day. Ears of mice from this experiment were used to analyze the gene expression of TSLP and IL-4. It was found increase gene expression of TSLP and IL-4 in cells of the mouse ears that were treated with MC903 mixed with ethanol while the cells of mouse ears treated with ethanol show no gene expression of TSLP and IL-4. Disparate effects of vitamin D result causing AD can be explained from differences in target cell populations. Systemically administered vitamin D can promote dendritic and regulatory T cell development, however, stimulation of keratinocytes (and dendritic cells) by topical application may override the immunosuppressive effects of vitamin D, thus promoting an allergic answer. Taken everything together we can conclude that topical application of vitamin D on skin can induce AD.