MG is well-characterized at the effector stage with three autoantigens accounting for nearly 90–95% of the clinical cases; the major target, in 80–85% of MG patients, is the muscle acetylcholine receptor (AChR) [2], whereas in the rest of the MG patients, pathogenic autoantibodies are directed towards the muscle-specific tyrosine kinase (MuSK) [3] or the low-density lipoprotein receptor-related protein 4 (LRP4) [4, 5]. Here, LRP4 is linked to myasthenia gravis.