Possible mechanisms include: (1) to inhibit inflammasome activation through estrogen receptor (71); (2) to repress HCC growth via inhibiting alternative activation of tumor-associated macrophages (72); (3) to inhibit HCC progression because of transition from pro-inflammatory to anti-inflammatory phenotype of Kupffer cell via the physical interaction between estrogen receptor alpha and NF-κB (73). The gene discussed is ESR1; the disease is hepatocellular carcinoma.