Short ReportsMyalgic Becker Muscular Dystrophy Due to an Exon 15 Point Mutation: Case Series and Literature ReviewTavallaee, Zachary OMS*; Hamby, Tyler PhD*,†; Marks, Warren MD‡ Author Information *Texas College of Osteopathic Medicine, University of North Texas Health Science Center, Fort Worth, TX; †Department of Research Operations, Cook Children's Health Care System, Fort Worth, TX; and ‡Department of Child Neurology, Cook Children's Health Care System, Fort Worth, TX. Reprints: Warren Marks, MD, Department of Pediatric Neurology, Cook Children's Health Center, 901 7th Avenue, Fort Worth, TX 76104 (e-mail: [email protected]). The authors report no conflicts of interest. Journal of Clinical Neuromuscular Disease 24(2):p 106-110, December 2022. | DOI: 10.1097/CND.0000000000000413 Buy Metrics Abstract Dystrophinopathies result from mutations to the DMD gene. We report 5 boys in 3 families with heterogenous phenotypes due to a point mutation in the DMD gene: a hemizygous tyrosine-to-cysteine change in exon 15 (c.1724T>C) resulting in an amino acid substitution of leucine to proline at codon 575. This mutation has been reported before, with at least 3 prior patients presenting with similar clinical findings of myalgia, myoglobinuria, and occasional muscle cramping. The mutation on DMD c.1724T>C (p.Leu575Pro) is listed in the Clinvar database as a variant of unknown significance. Our report provides contributing evidence that this alteration should be classified as pathogenic. Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.