Gibb and colleagues investigated if EAAT2 splicing could beinvolvedin the EAAT2 dysfunction in ALS.72 Usingthe SOD-1 mouse model, the authors observed that EAAT2 impairmentcould be linked to caspase-3 activation.72 Caspase-3 cleaved EAAT2 at the cytosolic C-terminal domain producingtwo fragments: (1) truncated EAAT2 and (2) carboxy terminus of EAAT2(CTE). The gene discussed is CASP3; the disease is amyotrophic lateral sclerosis.