In the context of familiar ALS, it has been reported that mutations in genes such as superoxide dismutase 1 (SOD1) and TAR DNA-binding protein 43 (TARDBP) promote microglia activation [27] through nuclear factor-kappa B (NF-κB) and NLRP3 pathways [28], while mutations in chromosome 9 open reading frame 72 (C9orf72) [23], TANK binding kinase 1 (TBK1) [29], and optineurin (OPTN) [30] affect the inflammatory type I interferon response. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.