Atopic dermatitis (AD) (syn. atopic eczema) is a chronic inflammatory skin condition, affecting up to 20% of children and 5%-10% of adults. 1,2 Current understanding of AD pathogenesis points towards a sophisticated interplay between genetic and environmental factors. The pathogenesis of AD may start in many cases with a genetically predetermined skin barrier defect, which manifests itself as dry skin. This inherent skin barrier deficit leads to an overexpression of pro-inflammatory cytokines and subsequently the activation of innate lymphocyte subsets and antigen-presenting cells (T H 2 and T H 22). IL-4 and IL-13 in particular drive eosinophil and mast cell recruitment and IL-31 secretion, a key cytokine involved in itch sensation. 3 Transcutaneous sensitization to environmental allergens and bacterial infections, in particular Staphylococcus aureus, further contributes to the barrier disruption and eczematous skin inflammation. While a genetic barrier defect is present in many, this is not a prerequisite and many pathological pathways can lead to AD. There