In ER+breast cancer, KLF9 may enhance the anti-tumor effect by cooperating with GR, activate GR dependent growth suppressor genes (such as GILZ) and integrate estrogen signal feedback regulation to achieve proliferation inhibition; In TNBC, KLF9 directly inhibits the NF - κ B-MMP9 signaling axis through epigenetic silencing mechanisms (such as recruiting HDAC1 to the target gene promoter region) and antagonizes the GR driven pro cancer MAPK/STAT3 pathway, thereby inhibiting metastasis. Here, HDAC1 is linked to breast carcinoma.