However, suppression of Drp1 activation by transfection with shDrp1 or shFis1, and treatment with a chemical inhibitor (Mdivi-1), consistently prevented the mitochondrial fragmentation induced by ALS-related mutations, suggesting that Drp1-Fis1 signaling is necessary for ALS-related mitochondrial fragmentation (Fig. 2a and Supplementary Fig. 1a). The gene discussed is DNM1L; the disease is amyotrophic lateral sclerosis.