Given the strong evidence supporting the role of TREM2 and DAP12 as inhibitors of TLR signaling [67], it is possible to hypothesize that amyloid-stimulated TLR activation is disinhibited in NHD, with consequent excessive microglial activation and reduced ability to phagocytose amyloid deposits or apoptotic neurons. Here, TYROBP is linked to Nasu-Hakola disease.