In agreement with this study, Grn KO mice showed lysosomal dysfunction, including lipofuscin deposits and defects in lysosomal turnover (Ahmed et al., 2010; Wils et al., 2012); moreover, FTD patients with GRN mutations exhibit lipofuscin deposits in their cortex and retina and fibroblasts derived from these patients have decreased lysosomal protease activity (Ward et al., 2017). The gene discussed is GRN; the disease is frontotemporal dementia.