SOD1 and amyotrophic lateral sclerosis: However, given our previous functional analysis of activity dependent Ca2+ homeostasis in hMNs from SOD1G93A mice (Fuchs et al., 2013) and the fact that none of the recently generated models was shown to recapitulate most aspects of human ALS as convincing as the SOD1 mutant mouse, we continued to focus on the analysis of SOD1G93A mice in this complementary study.