Lu et al. (2020) found that when miR-4425 mimics or FDFT1 siRNA were transfected into 20(S)-Rg3-treated ovarian cancer cells they could counteract the anti-tumor activity of the ginsenoside Rg3. Their study showed that Rg3 exerted anti-ovarian cancer activity by down-regulating the expression of oncogene miR-4425, thereby affecting the expression of FDFT1. Although accelerated cholesterol metabolism is associated with cancer development and progression, it is inconclusive whether FDFT1 is a tumor-suppressor gene or a candidate oncogene (Weng M. L. et al., 2020). The gene discussed is FDFT1; the disease is neoplasm.