In summary, the author of this manuscript proposes based on the work of Seki et al. that the SOD1G93A mutation-induced oxidative damage leading to abnormal protein synthesis could lead to Nav1.6 Na+ channelopathy in the Mes V neurons of a mouse model for ALS only after earlier primary microdamage, namely the lost function of Piezo2 and associated Nav channelopathies that lead to the proposed progressive proprioceptive terminal detachment in ALS. The gene discussed is SCN8A; the disease is amyotrophic lateral sclerosis.