The observation that TBK1-E696K mutant that causes ALS-FTD constitutively localizes to lysosomes, phosphorylates Rab7 and enhances mTORC1 amino acid responsiveness strengthens the link between lysosomal TBK1 and mTORC1 activation and suggests a possible neurodegenerative disease relevance. Here, RAB7A is linked to frontotemporal dementia.