TARDBP and amyotrophic lateral sclerosis: The C-terminal glycine-rich domain (also termed the intrinsically disordered or low complexity domain) mediates protein–protein interactions (Ayala et al., 2008; Buratti and Baralle, 2012; Budini et al., 2012) and harbors most, but not all, familial TARDBP mutations that are causative for FTLD/ALS (Pesiridis et al., 2009; Sreedharan et al., 2008).