Atopic dermatitis (AD) is a chronic inflammatory skin disorder and the most frequent skin disease in children. Skin barrier defects play a crucial role in its pathogenesis. 50% of patients suffering from AD present mutations in the filaggrin gene, coding for a key protein of the upper layer of the skin. However these mutations alone are not sufficient for disease development, suggesting that environmental factors are also of great importance in the genesis of AD. In particular skin infections frequently provoke clinical exacerbations in patients suffering from AD. New insights into skin barrier dysfunctions have facilitated the development of drugs targeting the sustainable restitution of the skin's physiologic function. These agents could modify the pharmacological approach of AD treatments in the future.