In SOD1G93A mice, neurodegeneration was prevented by overexpression of BCL2 and by delaying caspase activation, highlighting the importance of apoptosis in ALS.483 On the other hand, deletion of BAX improved the lifespan of SOD1G93A mice.484 Also, BIM targeting has been proposed as a potential strategy for ALS as upregulation of BIM in an ALS mouse model has been observed. Here, BAX is linked to amyotrophic lateral sclerosis.