While our data support that neurodegenerative processes are mediated by the circadian clock in spinal cord cholinergic neurons—the cell-type of ALS disease pathogenesis—further investigation into how Bmal1 loss influences the localization and function of ALS-linked RBPs (e.g., TDP-43 and FUS) would help establish a link between clock disruption and ALS-specific pathophysiology. The gene discussed is TARDBP; the disease is amyotrophic lateral sclerosis.