This phenomenon may be associated with estrogen levels, which play an important role in thyroid cancer cell proliferation through binding to nuclear receptors estrogen receptor α (ERα) and estrogen receptor β (ERβ), as well as by activating various signaling pathways (e.g., AKT/mTOR, MEK1/2, and MAPK) to stimulate thyroid cancer cell growth (21–23). This evidence concerns the gene AKT1 and thyroid cancer.