From UCA1 knockdown and overexpression experiments in breast cancer cells, such as MCF7, T47D, and tamoxifen-resistant cells derived from these cells, it has been suggested that UCA1 enhances tamoxifen resistance by activating the mammalian target of rapamycin (mTOR), Wnt/β-catenin, and PI3K/AKT signaling pathways (Figure 3A) [53,54,55]. The gene discussed is AKT1; the disease is breast carcinoma.