In the normal development and maintenance of the neuromuscular junction (left), structural organization is maintained thanks to signaling by proteins such as muscle-specific kinase (MuSK), Vangl2, and Wnt ligands, researchers propose. In mice whose muscles don’t produce Vangl2 (right), junctions are instead disorganized. Compared with control animals, mice lacking muscle Vangl2 have more-dispersed postsynaptic acetylcholine receptors, muscles that are withdrawn, and a reduction in synaptic transmission. As a result, the muscles aren’t properly innervated and mice experience muscle weakness.