To determine the relative contribution of TLR2 and TLR4 in diabetic nephropathy, Mudaliar et al. further showed that, in vitro, both TLR2 and TLR4 could be stimulated by HMGB1 and mediate NF-κB activation, but only TLR2 expression, not TLR4, was sustained for 7 days under high glucose conditions, implying that long-term pro-inflammation merely depended on TLR2 in diabetic nephropathy (17). Here, NFKB1 is linked to diabetic kidney disease.