The study concluded that the decreased IgM/IgG antibody response to α-Gal observed in GBS patients could reflect a dysbiosis of the gut microbiota associated with infection with pathogens that trigger neuropathy, and that GBS should not be considered a factor that increases anti-α-Gal IgE levels and, therefore, the risk of tick-bite-related allergies [22]. The gene discussed is CD40LG; the disease is infection.