JAK-inhibitor therapy resolves atopic dermatitis and abrogates hyperactive STAT phosphorylation in whole blood. (a–f) Severe atopic dermatitis in P3 (a) before (SCORAD = 60) and (b) after (SCORAD = 16) 30 days of in vivo treatment with baricitinib. Levels of pSTAT1 (c), pSTAT3 (d), pSTAT5 (e), and pSTAT6 (f) from P3 (E139K), who were treated with baricitinib in vivo. Results depicted as pretreatment (pre-) and posttreatment (post-) levels of pSTATs in granulocyte subsets, B cell subsets, major T cells subsets, CD4+ T cells subsets, CD8+ T cell subsets, NK cells subsets, dendritic cell subsets, and monocyte subsets. Results represented as fold-change in mean signal intensity (FCMSI) compared with non-treated HC (n = 1 for pre-treatment run and n = 1 for post-treatment run). For all panels, CM = central memory; EM = effector memory; TEMRA = T effector memory CD45RA+; NK = natural killer, DC = dendritic cell. Populations labeled “granulocytes” comprise all CD66b+ cells (including neutrophils, eosinophils, and basophils).