The authors demonstrated an inverse correlation between Mfn2 and miR-125a levels in pancreatic cancer cells; moreover, Mfn2 was validated as a miR-125a direct target, and as a consequence, miR-125a replacement triggered excessive mitochondrial fission via its downregulation, leading to activation of mitochondria-associated apoptosis, with MOMP dissipation and subsequent cytochrome c leakage. This evidence concerns the gene MFN2 and pancreatic neoplasm.