Although these antipruritic benefits may partly reflect baseline differences or prescribing patterns in clinical practice, the consistent and greater improvement in pruritus observed with JAK1i suggests a potentially more effect on itch pathways, particularly those involving IL-31—a key mediator of pruritus in AD not targeted by IL-13Ab (13–15) —as well as its broader inhibition of key Th2-related cytokines such as IL-4 and TSLP (6, 16–18), resulting in enhanced antipruritic efficacy. This evidence concerns the gene IL31 and Alzheimer disease.