LAUSR

additional insights into the pathogenesis of myasthenia gravis (1). In essence, they applied Mendelian randomization to genome-wide data that we made for a large cohort of patients diagnosed with the neuromuscular disor-der (2). This powerful approach identi fi ed genetic variants increasing the risk of developing myasthenia gravis by in fl uencing gene expression. Their most exciting observa-tions centered on CHRNB1 and ERBB2 , two loci we discov-ered in our genomic and transcriptomic analyses (2). Their data corroborated our conclusions in that they found rs4151121 to in fl uence the expression of CHRNB1 in skeletal muscle. ERBB2 was also implicated in their search, though the lead variant and tissue involved differed between the two studies. We had identi fi ed rs2102928 in skeletal muscle as the candidate variant affecting ERBB2 expression, where-as rs1565922 in peripheral nerves was implicated in this current analysis. These fi ndings are not mutually exclusive and point to this myasthenia gravis – related gene operating across multiple tissues.