Thus, the downregulation of Mfn2 and Opa1 and overexpression of Fis1 observed in BD patients can induce mitochondrial fission and apoptosis because mitochondrial fragmentation induced by Fis1 is followed by cytochrome c release, caspase activation and cell death.64 Taken together, we suggest that an imbalance in mitochondrial fission and fusion towards fission causes mitochondrial fragmentation and may drive the cell into apoptosis, leading to the release of pro-apoptotic proteins, cristae remodeling, and activation of caspase-3. This evidence concerns the gene MFN2 and Behcet disease.