In the first model, mice carried the hSOD1(G93A) mutant under the control of the skeletal muscle-specific promoter from rat myosin light chain (MLC)-1, resulting in higher expression of the MLC/SOD1(G93A) transgene in muscles enriched in fast fibers (the most damaged in ALS), and lower in slow muscles such as the soleus, of adult mice [128]. Here, SOD1 is linked to amyotrophic lateral sclerosis.