Advances in research into the molecular basis of host and microbe interactions on the skin has enabled significant progress towards understanding the pathogenesis of atopic dermatits. We now understand that AD is driven by defects in the epidermal barrier that are linked to dysfunction of specific elements of the skin microbiome. Defects in the host and the resident microflora combine to drive immune dysfunction and establish a chronic cycle of disease. This presentation will provide an update of our latest work that has defined a targeted approach to correction of the microbial dysfunction associated with AD, and successful translation of this information into human therapy.