For instance, targeting TREM1, inhibiting S100A8/A9 activity, or blocking key inflammatory pathways (e.g., NF-κ B) or their downstream effectors (e.g., CXCL8, MMP9) could represent novel strategies to mitigate excessive inflammation and tissue damage in mastitis, providing a theoretical basis for clinical management and breeding of disease-resistant dairy cows. The gene discussed is IGKV1D-22; the disease is mastitis.