In line with our findings, targeting the mitochondrial fission regulator protein, DRP1, via genetic depletion, and pharmacological inhibition, using Mdivi-1 abolished brain tumor initiating cells [69], impaired FAO and thus reduced breast cancer brain metastases [11], suggesting that DRP1-mediated mitochondrial plasticity is essential for tumor progression. The gene discussed is DNM1L; the disease is brain neoplasm.