STING1 and Alzheimer disease: They displayed delayed wound healing and showed several characteristic features of atopic dermatitis (AD) even in the absence of injury, including keratinocyte hyperproliferation, an impaired epidermal barrier due to diminished expression of tight junction components, overexpression of pro-inflammatory cytokines and of interferon-stimulated genes (ISGs) and an immune cell infiltrate similar to the one observed in AD.14