CASC2 in serum and renal tissue was specifically downregulated in patients with type 2 diabetes with podocyte injury [23], and CASC2 upregulation suppressed proliferation, the accumulation of extracellular matrices, and oxidative stress in mesangial cells through the miR-133b/FOXP1 regulatory axis [15]. This evidence concerns the gene FOXP1 and type 2 diabetes mellitus.