Atopic Dermatitis affects both children and adults and is a serious health concern in many countries. AD is a complex disease with host and environmental factors underlying its pathology. Its treatment is multidimensional reflecting the diverse nature of its triggers and includes emollients, topical steroids and calcineurin inhibitors among others. Immunological dysfunction can be addressed broadly with systemic immunosupressors and specifically with monoclonal antibodies. Dupilumab, which targets IL-4 and IL-13 was granted approval for treatment of moderate-to-severe AD. Biologics targeting IgE/Th2 pathways may have its role in patients with overlapping AD and asthma. Psychological distress can exacerbate symptoms and is associated with increased severity of AD. Environmental triggers, such as, allergens can be addressed in selected cases with allergic immunotherapy. In this paper, we discuss AD treatment and propose a new step-by-step approach aiming at maintaining disease control and improving quality of life. ty is associated with various inflammatory conditions, including asthma and allergic diseases. As such, a fundamental role for microorganisms in human health, whether indigenous or environmental, is becoming increasingly evident. Besides the importance of the environment in the development of allergic diseases, an increased familiar predisposition for the development of these conditions may exist. This observation led researchers to hypothesize that host genetic factors could be involved in the pathogenesis of AD. The description, back in 2006, that loss-of-function mutations in the filaggrin (FLG) gene were a strong genetic risk factor for AD, became a significant breakthrough regarding prognosis and treatment. FLG monomers aggregate keratin filaments into tight bundles, resulting in the collapse and flattening of corneocytes that maintain both skin barrier integrity and normal stratum corneum (SC) lipids. Therefore, mutations in the FLG gene may increase skin permeability, predisposing individuals to skin allergen penetration and subsequent infection. These mutations have also