Given that actin filaments also participate in the transport of GLUT4 traffic [62, 63], the cytoskeleton rearrangement caused by ENST00000436340-induced RAB3B inhibition may also be responsible for the reduction of GLUT4 translocation to the plasma membrane, revealing that regulation of GLUT4 subcellular localization is a potential therapeutic strategy against insulin resistance in DKD. This evidence concerns the gene SLC2A4 and diabetic kidney disease.