Indeed, an ALS-related TBK1 mutant deprived of amino acids 690–713 in the CCD2 domain was shown to be unable to bind OPTN when transiently overexpressed in HEK293T cells while preserving interaction with other TBK1 protein partners (Freischmidt et al. 2015). The gene discussed is TBK1; the disease is amyotrophic lateral sclerosis.