This interaction induces conformational changes in STING, triggering downstream signaling cascades, including the activation of IRF3 and the phosphorylation and nuclear translocation of NF‐κB.[11] In eukaryotic cells, the nucleus and mitochondria are the exclusive compartments for DNA, both of which undergo intense oxidative stress during AKI, leading to the production of substantial oxidative‐DNA fragments. The gene discussed is NFKB1; the disease is acute kidney injury.