Although glucose concentration levels have not been investigated in muscles of SOD1(G86R) ALS mice, an excess of glycogen associated with an inhibited glycolysis has been found in the tibialis of these mice (Palamiuc et al., 2015), suggesting a defect in glucose availability for ALS muscle, even in a context of an excessive glucose uptake (Fergani et al., 2007). The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.