Figure 2 illustrates the role of IL-37 in AD. The secretion of IL-37 by peripheral blood mononuclear cells (PBMCs) exhibited a notable decrease subsequent to stimulation with recombinant Th2 cytokines [28]. Conversely, there was no observable alteration in IL-37 production following stimulation with Th1 cytokines [28]. This observation implies that the Th2 immune response has the capacity to inhibit the production of IL-37 [28]. The gene discussed is IL37; the disease is Alzheimer disease.