Beyond antiganglioside antibodies that featured GBS, a growing number of molecules are potential biomarkers of GBS (8), including infection trigger-associated surface molecules (e.g., lipo-oligosaccharides of Campylobacter jejuni), active components of immune systems (e.g., FcγR/FcRL gene polymorphism, cytokines, complements, chemokines), brain-derived proteins (e.g., total protein, albumin), and neuronal composition (e.g., neurofilaments) (9–11). This evidence concerns the gene FCRLA and Guillain-Barre syndrome.