In AD, the JAK-STAT pathway seems to exert a relevant role in reducing inflammation, pruritus and regulating filaggrin expression89, 90; IL-4, IL-5, IL-13, IL31, IL-22, and thymic stromal lymphopoietin (TSLP) bind to JAK-STAT–dependent receptors, activating the JAK-STAT cascade (via JAK1-3 and TYK2), therefore upregulating the inflammatory cytokines.11, 91 Inhibition of the JAK-STAT pathway proved to be an efficacious therapeutic target in inflammatory diseases, and oral JAK inhibitors may exert selective, fast and reversibly blockage of the Th2 cytokine and B-cell mechanisms involved in AD. The gene discussed is SOAT1; the disease is Alzheimer disease.