AD itch results from dysregulation of neuro-immune circuits involving crosstalk between various receptors [TRP family members, Toll-like receptors, protease-activated receptor 2 (PAR2), IL-4R, IL-13R, IL-31RA, OSMR, Mas-related G proteins], itch peptides [substance P (SP), natriuretic peptide (BNP), and proteases], and pruritogenic cytokines [thymic stromal lymphopoietin (TSLP), IL-2, IL-4, IL-13, and IL-31] (11–13). The gene discussed is TSLP; the disease is Pruritus.