Among these, one of the striking observations is the differential expression of numerous ALS-linked genes (i.e., ANG, DCTN1, SQSTM1, and TBK1) involved in autophagy, a highly conserved and tightly regulated cellular self-degradative process whose alteration leads to an impaired clearance of toxic protein aggregates and/or of damaged mitochondria that represent some of the best characterized hallmarks of both SALS and FALS [61]. The gene discussed is TBK1; the disease is amyotrophic lateral sclerosis.