SPB was shown to extend survival and motor performance in transgenic ALS SOD1 animal model, and these effects were attributed to an upregulation in the expression of nuclear factor κB (NF-κB) and bcl-2 proteins41, although the genetic inhibition of NF-κB in SOD1 mice does not ameliorate disease onset and progression59. The gene discussed is BCL2; the disease is amyotrophic lateral sclerosis.