Although motor neurons have been successfully produced via differentiation of ALS-iPSCs, no reports indicated whether SOD1 mutation interferes with this differentiation. Therefore, Li et al. tackled this issue in 2015 (Li et al., 2015) whereby ALS-iPSCs were derived from fibroblasts using retroviruses. This was followed by differentiation into NPCs via EB formation assay by inhibiting the SMAD pathway. Interestingly, no significant differentiation differences were seen between control and SOD1-iPSCs, suggesting that SOD1 mutation has no obvious effects on neural induction. Moreover, NPCs were treated with fetal bovine serum (FBS) to induce astroglia formation, which successfully expressed the astroglia progenitor marker CD44. It is noteworthy mentioning that generation and maturation of iPS derived-astroglia takes a long time in vitro, providing a platform to screen drugs that may be used to enhance astroglia development and maturation (Li et al., 2015). Some late studies have also suggested a role for astrocyte pathogenesis in ALS that also express the mutant SOD1 gene contributing to the death of motor neurons (Di Giorgio et al., 2007; Nagai et al., 2007). This authenticates the importance of iPSCs
