NCL neuropathology is not yet confirmed in GRN-null patients [3] but inferred based on the consistency of clinicopathological features shared by GRN mutation carriers and patients with other genetic causes of NCL and the consistency of neuropathological features seen in other forms of NCL, their respective mouse models, and Grn-null mice (reviewed in [6]). The gene discussed is GRN; the disease is neuronal ceroid lipofuscinosis.