Considering that only approximately 20% EphA4 protein was detected in the brain and no EphA4 protein expression was found in the spinal cord after the EphA4-ASO treatment, such low level of EphA4 expression might be insufficient to maintain normal survival of motor neurons, protect them from death and subsequently improve functional performance in ALS disease progression, just like our homozygous deletion of EphA4 in ChAT-positive cells in SOD1G93A mice did. This evidence concerns the gene EPHA4 and amyotrophic lateral sclerosis.