We have previously shown that P110 treatment inhibits excessive activation of Drp1 by inhibiting the interaction between Drp1 and Fis1 on the mitochondria under stress conditions in neuronal cells and in models of Parkinson’s disease and Huntington’s disease [36, 58] and that P110 does not affect Drp1 interaction with any other mitochondrial adaptors of Drp1 or with the mitochondrial fusion proteins, Mfn1 or Mfn2. The gene discussed is DNM1L; the disease is juvenile Huntington disease.