Exaggerated inflammatory responses may result in widely diffused secondary changes that influence the AD phenotype, such as suppression of epidermal differentiation genes, including FLG, by Th2, Th22 and Th1 cytokines,28 as well as excessive degradation of FLG and disorders in the processing of profilaggrin, as described in mice and humans.29 The gene discussed is FLG; the disease is Alzheimer disease.