Nevertheless, our data from human cohorts; from cell models with PKCδ overexpression, downregulation, or pharmacological inhibition; and from mouse models with rottlerin treatment, consistently support that PKCδ is a specific biomarker for microglia‐mediated neuroinflammation and that inhibition of PKCδ may be a viable treatment strategy for Aβ‐induced neuroinflammatory damages in AD. This evidence concerns the gene PRKCD and Alzheimer disease.