The data presented thus far above show that SLC38A5, which is upregulated in TNBC, could provide selenium to cancer cells via the mediation of the cellular uptake of Se-Met and that Se-Met potentiates Nrf2 signaling with a resultant increase in the expression and function of SLC7A11 and glutathione-synthesizing machinery. The gene discussed is SLC7A11; the disease is cancer.