Another example of the oncogenic effect of T3 and THRα-1 is that increased signaling has been shown to increase levels of phosphorylated AKT in hepatocellular cancer, and since phosphorylated AKT is overexpressed in several cancers and is also associated with worse prognosis in breast cancer, it could be a possible mechanistic pathway of thyroid hormone receptor signaling in breast cancer as well [30, 31]. This evidence concerns the gene AKT1 and cancer.