The expression levels of aldose reductase, which is a source of the cytoprotective osmolyte sorbitol, was observed to be no different between untreated cells and cells exposed to hyperosmolar stress, probably due to permanent intracellular increased ionic stress and subsequent permanent activation of NFAT5 in DMD myoblasts [19]. The gene discussed is AKR1B1; the disease is Duchenne muscular dystrophy.