More recently, Dobrowolny et al. reported that muscle-restricted expression of IGF-1 isoforms maintained muscle integrity, stabilized neuromuscular junctions, reduced inflammation in the spinal cord, enhanced motor neuronal survival, and delayed the onset and slowed disease progression in sodium dismutase 1 (SOD1) G93A mice.12, 13 Both these studies reappraised the potential role of the skeletal muscle and IGF-1 signaling as a target for treatment in ALS patients. The gene discussed is IGF1; the disease is amyotrophic lateral sclerosis.