While other details of this process are subject of future studies, our finding that buffering of excess cytosolic Ca2+ improves repair of ANO5-patient muscle cells provides proof-of-principle for efficient removal of cytosolic Ca2+ in the muscle of ANO5 patients as a potential therapeutic strategy for treating LGMD2L and MMD3 patients. This evidence concerns the gene ANO5 and autosomal recessive limb-girdle muscular dystrophy type 2L.