As proof of concept that activation of Nrf2 might have a beneficial effect in human ALS, we were able to demonstrate that S[+]-apomorphine reduced pathologically elevated levels of oxidative stress in fibroblasts from patients with both mutant SOD1-related and sporadic ALS, and could reduce oxidative stress-induced cell death in this human cell model. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.