Although previous expression profiling studies have highlighted sub-groups of genes such as a set of innate immunity genes [12] and the “epidermal differentiation cluster” [14], or potential gene candidates including NELL2, CCL18, AQP3 and tenascin-C [42]–[44] that are deregulated in AE, the complete genome-wide picture of AE is still far from understood. Here, CCL18 is linked to acrodermatitis enteropathica.