Guillain–Barré syndrome (GBS) is an autoimmune disease characterized by progressive limb weakness, sensory deficits, cranial nerve involvement, tendon areflexia, and cerebrospinal fluid (CSF) albumin cytological dissociation with three major pathophysiological phenotypes: acute inflammatory demyelinating polyneuropathy (AIDP), acute motor axonal polyneuropathy (AMAN), and acute motor and sensory axonal neuropathy (AMSAN) (1). This evidence concerns the gene ALB and Guillain-Barre syndrome, familial.