MYMX (myomixer) is a fusogenic micropeptide essential for myoblast fusion and skeletal muscle development 1. It mediates the formation of multinucleated muscle fibers by generating membrane stresses via its extracellular C-terminus to drive fusion pore formation, acting independently of the related fusogen MYMK 1. During muscle regeneration, MYMX expression is promoted through a regulatory network involving lncRNA OIP5-AS1-mediated degradation of miR-7, which normally suppresses MYMX mRNA 2. MYMX dysfunction has significant clinical relevance: biallelic MYMX variants cause Carey-Fineman-Ziter syndrome (CFZS), presenting as congenital myopathy with hypotonia, facial nerve palsy, growth restriction, and dysmorphic features 13. Patient-derived myoblasts show defective fusion capacity that can be partially restored through CRISPR/Cas9-mediated base editing, indicating therapeutic potential 1. The gene is transcriptionally regulated during satellite cell activation as part of the myogenic program 4, and its expression is dysregulated in various neuromuscular conditions, including Duchenne muscular dystrophy where MyoD-controlled MYMX expression is downregulated 5. These findings establish MYMX as a critical myogenic fusion factor whose dysfunction contributes to hereditary neuromuscular disease pathogenesis.