Prior research has already confirmed that skeletal muscle mitochondrial dysfunction is involved in the severity and progression of ALS, and, as PGC-1α is implicated in mitochondrial biogenesis and function, the inhibition of this miRNA could be used to develop a therapeutic strategy to restore PGC-1α activity in ALS patients [67]. The gene discussed is PPARGC1A; the disease is amyotrophic lateral sclerosis.