In the early 2000s, αDG sugar chain abnormalities and loss of laminin-binding activity were reported in specimens of patients with Walker–Warburg syndrome (WWS), muscle–eye–brain disease (MEB), Fukuyama congenital muscular dystrophy (FCMD), congenital muscular dystrophy 1C, and limb-girdle muscular dystrophy (LGMD) 2I (alternatively called LGMDR9) [3,4,5,6]. Here, LAMB2 is linked to muscular dystrophy-dystroglycanopathy, type A.