Strategies employing Bcl-2 family-mediated apoptosis to treat amyotrophic lateral sclerosis (ALS) have been validated in ALS mouse models; the knockout of two Bcl-2 proteins, Bax and Bak, counteracts the toxic effects of mutant superoxide dismutase 1 (SOD1) by inhibiting the activation of pro-caspase-3, thereby preventing neuronal damage [369,370]. This evidence concerns the gene BAX and amyotrophic lateral sclerosis.