“…Although this has not yet been fully established for alopecia areata (AA), studies are now shedding light on immune pathways that are upregulated in this common, T-cell-mediated disease that has a lifetime prevalence of up to 2%, and is typified by nonscarring hair loss (Renert-Yuval and Guttman-Yassky, 2016). The AA phenotype shares some commonalities with AD, a remarkably prevalent inflammatory skin disease, including pruritus, elevated IgE levels, IL-13, and filaggrin mutations (Bakry et al, 2014;Betz et al, 2007;Finner, 2011;Jagielska et al, 2012;Suarez-Farinas et al, 2015). Furthermore, a history of atopy (personal or familial), and of AD in particular, is the greatest risk factor for the development of AA, and patients with AA who also have AD are at great risk for developing severe AA (Barahmani et al, 2009;Lee et al, 2014).…”