SOD1 and amyotrophic lateral sclerosis: Li et al. [91] showed that in male rNPCs, but not in female rNPCs, the overexpression of mutant SOD1 decreased significantly their proliferative and differentiating potential, and sensitivity to oxidative stress was increased, thereby suggesting that sexual dimorphism in ALS can be attributed to intrinsic cellular differences of sex and SOD1 G93A transgene, more than to gonadal steroids.