Importantly, accumulating evidence suggests that progranulin, a common genetic cause of FTD, and TMEM106B a major risk factor for FTD also have roles in endolysosomal function [7, 9, 16, 21, 34, 36, 37], with progranulin mutations leading to pathology reminiscent of lysosomal storage disorders [16]. Here, GRN is linked to frontotemporal dementia.