The increased expression of proapoptotic Bax, Bcl-2 homologous antagonist/killer (Bak) and activation of effector caspase-3 was also detected in the spinal cord of ALS patients, while the antiapoptotic Bcl-2 was decreased, supporting the activation of the apoptotic pathway [10]. This evidence concerns the gene BAK1 and amyotrophic lateral sclerosis.