In ALS patients, the following have been found: (i) elevated levels of excitatory amino acid present in CSF [251]; (ii) increased Ca2+ levels in motor nerve terminal [252]; (iii) loss of excitatory amino acid transporter 2 (EAAT2) in astrocytes, leading to increased extracellular glutamate concentration and neuronal excitotoxicity [253,254]; (iv) motor neurons that have scarce Ca2+ buffer systems and a high number of AMPA Ca2+-permeable receptors [255]. The gene discussed is SLC1A2; the disease is amyotrophic lateral sclerosis.