The current author postulates that the aforementioned progressive loss of Nav1.1 activity from intrafusal proprioceptive terminals due to irreversible loss of Piezo2 input could initiate the impairment of Nav1.6 Na+ channels in the SOD1G93A mouse model for ALS, as shown by Seki et al. [54]. The gene discussed is PIEZO2; the disease is amyotrophic lateral sclerosis.