Interestingly, overexpression of ALS in mice also caused 13% growth retardation in 4- and 8-week-old mice [118] showing that both the absence and very high levels of ALS lead to the same phenotype since IGF1 is either unprotected from proteolytic attack of IGFBP-3 proteases or sequestered into ternary complexes. This evidence concerns the gene IGF1 and amyotrophic lateral sclerosis.