Similarly, we have reported diminished TBK1/IFN-β pathway activation in both macrophages and microglia derived from an optineurin insufficiency mouse model (Optn470T), which does not bind ubiquitin due to a C-terminal truncation [23,24,25], thus mirroring some of the loss-off-function optineurin truncations found in ALS patients [13,26]. The gene discussed is OPTN; the disease is amyotrophic lateral sclerosis.