An increase in FUS-ALS MNs’ survival upon stimulation of glycolysis as well as a clear shift in metabolic rates in all cell cultures after their prolonged cultivation suggests that some compensatory upregulation of glycolytic pathways could be beneficial to ALS MNs, as was reported in fALS models for mutations in SOD1 and TDP43 genes [97]. The gene discussed is TARDBP; the disease is amyotrophic lateral sclerosis.