In fact, actin polymerization is required not only for GLUT4 transportation in muscle cells but also for clustering acetylcholine receptors at the neuromuscular junction66 and to recruit dysferlin to wounded areas of the sarcolemma67, supporting the idea that cytoskeletal actin disruption can lead to diverse muscle disorders by impairing intracellular trafficking. This evidence concerns the gene SLC2A4 and muscular disease.