The vast majority of these studies converge in a pro-oncogenic role of mitochondrial fission, as demonstrated by the therapeutic activity of Drp1 inhibitors or Mfn2 activators in preclinical models, although it also emerges that several cancer-related factors (genetic, metabolic, environmental) can affect the mitochondrial dynamics rheostat and its tumor modulating properties in a tissue-dependent manner [12,14]. The gene discussed is MFN2; the disease is cancer.