This dysfunction is directly linked to dystrophin deficiency, as the use of a read‐through compound (capable of bypassing the premature stop codon in the DMD gene) restored dystrophin expression in DMD astrocytes and rescued the glutamate uptake defect, preventing the associated neurotoxicity (Patel et al. 2019). The gene discussed is DMD; the disease is neuromuscular disease caused by qualitative or quantitative defects of dystrophin.