Indeed, it has been reported that AT-derived MSCs (AT-MSCs) administration into superoxide-dismutase-1 (SOD1)-mutant transgenic mice, the familial ALS mouse model, delayed the loss of motor neurons as well as increased the number of motor neurons in the lumbar region and also the expression levels of GDNF and basic fibroblast growth factor (bFGF) [33]. Here, SOD1 is linked to amyotrophic lateral sclerosis.