EIF2A and amyotrophic lateral sclerosis: A study by Wang et al. demonstrated that GBZ markedly inhibited GADD34-dependent eIF2α dephosphorylation, resulting in significant amelioration of disease onset, prolonged early phase of disease, and survival in a G93A transgenic mouse model of amyotrophic lateral sclerosis (ALS), as compared to G93A mice untreated with GBZ [281].