Mechanistically, activated HER2 induces the production of CCL2 (C-C Motif Chemokine Ligand 2) through the PI3K-NF-κB axis, promoting recruitment and activation of infiltrated immune cells (35), and TNBC patients were found to have a higher tumor mutation burden (TMB) and to present neoantigens that are correlated with a more effective immunotherapy response (36), while estrogen and estrogen receptor (ER) signaling appears to have little impact on the immune environment (37). The gene discussed is NFKB1; the disease is neoplasm.