Mechanistically, the secretion of PKCδ from microglia can be stimulated by Aβ, thus leading to upregulation of the NF-κB pathway, along with overproduction of proinflammatory cytokines; the authors therefore suggested that PKCδ may serve as a potential biomarker and therapeutic target for microglia-mediated neuroinflammation in AD [37]. The gene discussed is NFKB1; the disease is Alzheimer disease.