As an atopic disorder, AD is classically considered a type 2‐driven immunopathology involving type 2 T helper (Th2) cells, interleukin (IL)‐4, IL‐5, IL‐9, and IL‐13, as well as IgE, mast cells, basophils, and eosinophils—with more recent data expanding this view to include Th17 and IL‐22 cellular responses in the genesis of AD.12 While T cells are promoting inflammation in certain instances,13, 14, 15 they are largely dispensable in the Flgft/ft model. This evidence concerns the gene IL22 and Alzheimer disease.