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Affected individuals have variable clinical phenotypes but typically display both a decrement on repetitive nerve stimulation and myopathic findings on muscle biopsy. Inherited causes include myopathies related to mutations in <jats:italic>BIN1<\/jats:italic>, <jats:italic>DES<\/jats:italic>, <jats:italic>DNM2<\/jats:italic>, <jats:italic>GMPPB<\/jats:italic>, <jats:italic>MTM1<\/jats:italic>, or <jats:italic>PLEC<\/jats:italic> and congenital myasthenic syndromes due to mutations in <jats:italic>ALG2<\/jats:italic>, <jats:italic>ALG14<\/jats:italic>, <jats:italic>COL13A1<\/jats:italic>, <jats:italic>DOK7<\/jats:italic>, <jats:italic>DPAGT1<\/jats:italic>, or <jats:italic>GFPT1<\/jats:italic>. Additionally, a decrement due to muscle fiber inexcitability is observed in certain myotonic disorders. The identification of a defect of neuromuscular transmission in an inherited myopathy may assist in establishing a molecular diagnosis and in selecting patients who would benefit from pharmacological correction of this defect. Acquired cases meanwhile stem from the co\u2010occurrence of myasthenia gravis or Lambert\u2010Eaton myasthenic syndrome with an immune\u2010mediated myopathy, which may be due to paraneoplastic disorders or exposure to immune checkpoint inhibitors.<\/jats:p>","DOI":"10.1002\/mus.26676","type":"journal-article","created":{"date-parts":[[2019,8,26]],"date-time":"2019-08-26T16:14:41Z","timestamp":1566836081000},"page":"648-657","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":44,"title":["Trouble at the junction: When myopathy and myasthenia overlap"],"prefix":"10.1002","volume":"60","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5631-0559","authenticated-orcid":false,"given":"Stefan","family":"Nicolau","sequence":"first","affiliation":[{"name":"Department of Neurology Mayo Clinic  Rochester Minnesota"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Justin 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