In conclusion, our study elucidates a self-reinforcing inflammatory circuit in chronic endometritis, wherein STING-IRF7 activation drives dual pathogenic cascades:1) transcriptional upregulation of CD11b to amplify neutrophil recruitment, and 2) LCN2-MC4R-mediated ICAM-1 adhesion and NETosis, collectively fostering a microenvironment that suppresses HOXA10-the master architect of endometrial receptivity. The gene discussed is ICAM1; the disease is chronic endometritis.