In this study, utilizing a TwinF interface inhibitor, we have demonstrated that NMDAR-mediated glutamate excitotoxicity may be a significant contributor to RGC loss in ALS, since application of FP802 targeting the NMDAR/TRPM4 death complex could halt RGC loss in the SOD1G93A mouse model. This evidence concerns the gene TRPM4 and amyotrophic lateral sclerosis.