Here, we show that keratinocyte-specific deficiency of Ovol1 exacerbates AD-like inflammation induced by treatment with HDM and Staphylococcus aureus-derived toxin staphylococcal enterotoxin B (SEB), two environmental agents relevant to human AD pathogenesis [2] that are known to induce AD-like phenotypes in mice when used in combination [33]. The gene discussed is OVOL1; the disease is Alzheimer disease.