Similarly, in vivo data showed an increase in tubular TLR2, HMGB1, and fibronectin expression, with no increase in TLR4 expression, suggesting that the HMGB1-TLR2-NF-κB pathway might play a dominant role in mediating inflammation in diabetic nephropathy in the long term (17). Here, NFKB1 is linked to diabetic kidney disease.