The fact that IGF-1 treatment led to neuroprotection in an ALS animal model (Jablonka et al., 2011; Saenger et al., 2012) and to partial benefits in ALS clinical trials (Lai et al., 1997; Borasio et al., 1998), further supports our finding that up-regulation of IGF2 expression in the differentiated motor neurons from sporadic ALS patients highlights the importance of IGF family proteins as potential therapeutic targets for this disease. This evidence concerns the gene IGF1 and amyotrophic lateral sclerosis.