In the era of precision medicine, a systems biology approach merging the clinical phenotypes with biomarkers will be necessary to best exploit their potential significance for the molecular taxonomy of atopic dermatitis (AD). Cohort studies combined with environmental data and systems biology have proposed a novel approach to develop early indicators for the prediction, prevention, diagnosis, and personalized therapeutics for AD.
　　In our Childhood Environment and Allergic diseases Study (CEAS) cohort, we found that filaggrin P478S gene variants may confer susceptibility to the development of AD and may be modified by allergen sensitization levels. In addition to allergens, we discovered that exposure to endocrine-disrupting chemicals (phthalates) and tobacco smoke may increase the risk of AD via an adjuvant effect. We afford the evidence thatenvironmental exposures can induce epigenetic changes in gene expression and alter AD risk. Methylated TSLP 5′CGI may be a potential epigenetic biomarker for environmentally associated atopic disorders. Moreover, filaggrin variants may increase skin permeability leading to higher skin absorption of phthalates, and thus confer a higher susceptibility for AD. Many of the skin care products may contain phthalates but are not banned by current legislation. Thus, more attention should be paid to chemicals in skin care products especially for filaggrinvariant carriers.
　　Due to the hierarchical structures of the genetic and epigenetic alterations and the heterogeneity across patients, it remains as a challenge to obtain precise and comprehensive patient classifications that can be translated into customized therapeutics. To break through boundaries in precision medicine, advanced research on machine learning and artificial intelligence technologies for analyzing medical bioinformatics data will be a key component. Integrated precision medicine and chronic disease treatment models that enable patient self-care and shared decision making may improve medication adherence and outcomes for AD.