Here, we further prove that restoring mitochondrial network by either overexpression of fusion-related (Mnf1/Mnf2) proteins or inhibition of fission-related proteins (Drp1/Fis1) in diabetes-susceptible cybrids, impaired insulin signaling, and GLUT1/GLUT4 translocation to cell membrane can be repaired both in basal condition and in response to insulin stimulation. This evidence concerns the gene SLC2A1 and diabetes mellitus.