Notably, although the OPTN E50K mutation was proved to increase the binding ability of OPTN towards TBK1 (ref. 26), and the TBK1 E696K variation was reported to abrogate the interaction between TBK1 and OPTN19, the underlying mechanism governing the neurodegenerative diseases caused by these mutations are poorly understood. Here, OPTN is linked to neurodegenerative disease.