This is in line with the recent finding that OPTN forms a platform for TBK1 activation in which it engages with TBK1 in a positive feedback loop, and observations made with the ALS-causing TBK1-E696K mutant, which has lost its OPTN-binding capacity39,52,62 but not its binding to NAP1, as we show here. The gene discussed is TBK1; the disease is amyotrophic lateral sclerosis.