Both Sp1 upregulation in the spinal cord from symtomatic (4-month-old) SOD1-G93A mice, and the increase of nuclear immunolabelling for Sp1 in lumbar MNs preceding cell loss (3-month-old) underpin a key role for Sp1 in the ALS model (Fig. 7a, b). This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.