Mutations in both the carboxy-terminal domain of TBK1 and the amino-terminal domain of OPTN have been implicated in ALS and other neurodegenerative diseases (Maruyama et al. 2010; Pottier et al. 2015), and it is likely that disruption of the formation of the TBK1/OPTN complex impairs critical autophagy processes that are vital to maintaining cellular homeostasis (Li et al. 2016). The gene discussed is OPTN; the disease is amyotrophic lateral sclerosis.