Interestingly, LanCL1 has been shown to be vital for neuronal development and has been implicated in mitigating oxidative stress in the brains of mouse models.20 It has also been shown that LanCL1 overexpression promotes neuron survival in ALS mouse models,21 and it is naturally upregulated in the brains of mice treated with MPTP, a parkinsonian neurotoxin.22 These indications of an important role for LanCL1 in murine brain model systems suggest that DHAAs are present in mammalian brain samples and that glutathionylation of DHAAs has a neuroprotective role. The gene discussed is LANCL1; the disease is amyotrophic lateral sclerosis.