Recently, multiple reports suggested that the loss function of ADO production was at least in part related to the onset of autoimmune disorders (ie multiple sclerosis, encephalomyelitis, rheumatoid arthritis, diabetes and uveitis).43 More importantly, locally ADO production played a crucial role in stimulating the release of anti‐inflammatory cytokines (ie IL‐10) and inhibiting the release of proinflammatory molecules (ie TNF‐α and nitric oxide) in animal models of inflammation (ie myocardial infarction). This evidence concerns the gene ADO and multiple sclerosis.