Reviews highlight that astrocytic glutamate transporters (GLT-1/EAAT2 and GLAST/EAAT1) are critical for glutamate homeostasis, and their dysregulation contributes to excitotoxicity in ALS and Alzheimer’s disease; while direct CRISPR-mediated upregulation of these transporters is a promising strategy, most published work to date has focused on pharmacological or transcriptional modulation [64,65]. The gene discussed is SLC1A2; the disease is early-onset autosomal dominant Alzheimer disease.