In this study, we have shown that ephrinB2 protein expression is significanty increased in the lumbar spinal cord of postmortem samples from human ALS donors with an SOD1 mutation compared to non-diseased human samples, suggesting that this disease mechanism is also relevant to the human condition and is not restricted to only the mutant SOD1 mouse model. The gene discussed is EFNB2; the disease is amyotrophic lateral sclerosis.