Although IL-17 is not as predominant in AD as it is in psoriasis, studies have revealed that IL-17 can stimulate the differentiation of B cells into IgE-producing plasma cells, promote the release of IL-8, TNF-α, and TSLP, activate keratinocytes to express adhesion molecules, and modulate the Th2 immune response, thus triggering the chronic phase of AD (29–31). The gene discussed is TNF; the disease is Alzheimer disease.