Our finding of a significant reduction of IFN-γ compared to controls after adjustment for comorbidities and treatments is intriguing and in contrast with previous data from smaller case-control studies showing elevated IFN-γ levels in postmortem spinal cord, CSF, and serum from patients with ALS.18,23 Our observation may be explained by the relocation of IFN-γ-secreting Th1 cells into the CNS24 or by the upregulation of IFN-γ receptor in the CNS in response to the high levels of TNF-α and IL-1.25,26. The gene discussed is IFNG; the disease is amyotrophic lateral sclerosis.