Independently of the filaggrin study, it was demonstrated earlier that a disrupted barrier function of the stratum corneum is present in atopics not only in involved skin, but also in uninvolved dry skin facilitating permeation of various environmental substances into the skin (Berardesca et al., 1990; Werner et al., 1985; Watanabe et al., 1991; Loden et al, 1992). As a biomarker, an increased level of transepidermal water loss (TEWL) can be demonstrated (Tagami et al., 1985; Ghadially et al., 1996). Various functional and morphological studies on atopic xerosis that clinically appeared without inflammation demonstrated that cellular inflammation is already present in atopic skin and a key and initial step in the development of atopic dermatitis (Watanabe et al., 1991; Uehara et al., 1984). In fact, barrier dysfunction, atopic immune dysregulation, and atopic dermatitis pathogenesis are not independent events, but closely linked (Biedermann 2006; Hudson 2006). Th2 lymphocytes dominate the atopic immune phenotype and are the underlying cell type responsible for the induction if IgE antibodies (Biedermann et al. 1999, 2004). Barrier dysfunction predisposes for the development of Th2 lymphocytes and Th2 cells are the first cell type invading atopic skin initiating inflammation and the inflammatory vicious circle of inflammation (Biedermann 2002; 2004; Lametschwandtner et al. 2004; Günther et al. 2005). Next to Th2 lymphocytes, in atopic dermatitis skin lesions, infiltrates of eosinophils and cells of the mononuclear phagocyte lineage are found.