The pathophysiology of AD is complex and multifactorial, and an interplay between skin barrier dysfunction, occasionally caused by loss-of-function variants of the filaggrin gene, and an enhanced type 2 immune response, represented by an increase in IL-4, IL-13, IL-31, IL-33, and thymic stromal lymphopoietin, plays a central role in the development of the disease [1,2,3]. Here, IL4 is linked to Alzheimer disease.