Mice heterozygous for GRN mutations (GRN+/−) have been reported to exhibit subtle behavioral abnormalities but not the pathological hallmarks of GRN‐related neurodegenerative disease, likely because the mouse lifespan does not allow for the development of the sequelae of GRN haploinsufficiency, which manifest after several decades in humans.15, 16, 17, 18. The gene discussed is GRN; the disease is neurodegenerative disease.