This could be achieved by (1) targeting mediators of synaptic homeostatic processes activated in ALS-like mice, such as Scnn1a (Orr et al., 2020), and (2) targeting ion channels implicated in LVPN hyperexcitability in ALS-like mice, such as Nav1.6, HCN or KCNQ channels (Buskila et al., 2019; Saba et al., 2019). This evidence concerns the gene SCNN1A and amyotrophic lateral sclerosis.