In cisplatin-induced AKI, this pathway critically mediates cisplatin-triggered mtDNA leakage into tubular cytosol through BCL-2-like protein 4 (BAX) pores, activating the cGAS-STING/TBK1/NF-κB p65 axis that exacerbates post-injury inflammation in proximal tubular cells, whereas STING knockout attenuates neutrophil migration and ameliorates tubular inflammation (102). Here, NFKB1 is linked to acute kidney injury.