By activating the NF-κB pathway, this axis drives autophagy and epithelial-mesenchymal transition (EMT), directly contributing to stone-related renal injury while establishing a molecular bridge between crystal deposition and fibrotic progression (73).Further investigation of this mechanism may clarify chemokines’ dual roles in secondary stone injury and reveal CXCL12’s underappreciated contributions to Calcium Oxalate Nephrolithiasis. The gene discussed is NFKB1; the disease is nephrolithiasis susceptibility caused by SLC26A1.