Furthermore, Fatostatin can induce ER degradation by polyubiquitination of K48 junctions, a key mechanism for tamoxifen to inhibit PI3K-AKT-mTOR signaling in breast cancer, and has a synergistic effect with tamoxifen in reducing cell proliferation in vitro and in vivo tumor growth in breast cancer, indicating that Fatostatin may have promising clinical use for ER-positive breast cancer patients (Liu et al., 2020). The gene discussed is MTOR; the disease is breast cancer.