Our previous study demonstrated that DEK overexpression resulted in significant mitochondrial dysfunction in asthma, characterized by upregulation of Drp1, downregulation of p‐Drp1(637) and mitochondrial fusion protein 2 (MFN2), loss of mitochondrial membrane potential, excessive generation of mitochondrial ROS, and mitochondrial incompleteness.18 This evidence concerns the gene MFN2 and asthma.