Androgen/androgen receptor signaling is known to be involved in the initiation of carcinogen-related or HBV-related HCC in men [11], whereas estrogen has been shown to exert protective effects against HCC through interleukin-6 (IL-6) restraints, STAT3 (Signal Transducer and Activator of Transcription-3) inactivation, and tumor-associated macrophage inhibition [12–15]. This evidence concerns the gene STAT3 and neoplasm.