In addition to the effect of ganglioside antibodies on the integrity of myelin sheaths, cytokines [such as interferon-γ, tumor necrosis factor α (TNF-α), and interleukin 17 (IL-17)] (18, 19) and oxidative stress [such as the production of large amounts of reactive oxygen species (ROS) in cells] (20, 21) were also directly involved in the pathological process of demyelination in patients with GBS and CIDP, which are also associated with the occurrence of autoimmune thyroid disease and elevated TPO-Ab antibody levels (22, 23). This evidence concerns the gene IL17A and Guillain-Barre syndrome.