Further study revealed that upregulation of CD32b in the diabetic kidney of db/db mice was associated with higher levels of phosphorylated p65 subunit and its nuclear translocation, which was further enhanced in CRPtg-db/db mice (Fig. 5), suggesting that CRP may promote renal inflammation in T2DN via a CD32b-NF-κB signaling mechanism. Here, NFKB1 is linked to inflammatory response.