Another hallmark of AD is skin dysbiosis, with a shift toward a pathogenic microbiome, in which beneficial commensals such as Propionibacteria or Staphylococcus epidermidis are displaced by other species such as S. aureus, and the patients’ overall skin microbiota diversity decreases.29, 30, 31, 32 Results from flaky tail mice (Flgft/ftTmem79ft/ft) suggested that the microbiota promotes upregulation of IL‐17A and the infiltration of neutrophils and eosinophils into the skin.33 The gene discussed is IL17A; the disease is Alzheimer disease.