In addition, a study by Yang et al. identified that 17β-estradiol (E2) could attenuate the progression of HCC through the regulation of macrophage polarization, as E2 rechallenge reduced tumor growth in both orthotopic and ectopic mouse models of HCC, which functions as an inhibitor of alternative macrophage activation and tumor progression by keeping the estrogen receptor-β away from interacting with ATP5J and by interfering with the JAK1-STAT6 signaling pathway (Yang et al., 2012). This evidence concerns the gene STAT6 and neoplasm.