PIEZO2 and amyotrophic lateral sclerosis: 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.