A possible explanation for the feedback loop of AD inflammation indicates that IL-4, a Th2 cytokine, is involved in IL-31RA expression, increasing the production of the chemokines CCL17 and CCL22 by bone marrow-derived dendritic cells (BMDCs) and, together with external stimuli of the host’s defense, drives to a Th2 axis [30]. The gene discussed is IL4; the disease is Alzheimer disease.