Another three studies on different dermatitis, including atopic dermatitis, psoriasis, and epidermodysplasia verruciformis, indicated that S100A8/A9 were upregulated in keratinocytes in response to pathological stimulations and they formed heterodimer to contributed greatly to cell migration and inflammation in dermal keratinocytes [14, 15]. This evidence concerns the gene S100A8 and atopic eczema.