In addition, HG induced high-expression SOCS protein to inhibit the phosphorylation of JAK 2/STAT1/STAT3 and STAT transcriptional activity in human mesangial cells (HMCs) and in human proximal tubular (HK-2) cells, proving that SOCS protein can negatively regulate the JAK/STAT pathway and lessen inflammation, fibrosis, and abnormal cell proliferation that are present in DKD (Ortiz-Muñoz et al., 2010). This evidence concerns the gene SOAT1 and diabetic kidney disease.