Remarkably, the study further showed that, in TBK1 deficient mice, the reduced myeloid expression of TAK1—an endogenous RIPK1 inhibitor—promoted the key ALS/FTD phenotype hallmarks, including microgliosis, TDP-43 aggregation, neuronal loss, and behavioral deficits [27]. Here, RIPK1 is linked to amyotrophic lateral sclerosis.