SOD1 and amyotrophic lateral sclerosis: Inoue et al. [37] demonstrated that suppressing caspase-9 by overexpressing XIAP in motor neurons effectively slowed the progression of ALS in G93A SOD1 Tg mice, while Reyes et al. documented that neuron-specific deletion of BCL-associated X protein (BAX) or BCL2-homologous antagonist/killer (BAK), which are both proapoptotic BCL-2 family proteins, delayed the onset and extended the longevity of disease in the same mice [38].