Another study also proved that cGAS-STING was activated in DN and promoted the damage of DN podocytes, which was caused by activation of the NF-κB pathway downstream of cGAS-STING, but not IRF3, one reason being that IRF3 phosphorylation or IFN-β levels remain unchanged in DN mice. This evidence concerns the gene NFKB1 and liver dysplastic nodule.