Of note, Grn−/− mice exhibit pro-inflammatory microglial activation downstream of NF-κB signaling175,176 coupled with the acquisition of an FTD-associated microglial state that: (1) is different from the AD- and ALS-associated DAMs, and (2) actively supports neurotoxic TARDBP granule deposition177, at least in part as a consequence of lysosomal dysfunction178. The gene discussed is GRN; the disease is frontotemporal dementia.