BER displayed a tendency to ameliorate the inflammation resulting from DM via various pathways, e.g., suppression of phosphorylated Toll-like receptor (TLR) and IkB kinase-β (IKK-β) that is responsible for NF-κB activation; thus, BER interferes with the serine phosphorylation of IRS and diminishes insulin resistance [106]. This evidence concerns the gene NFKB1 and Insulin resistance.