We found that Erastin treatment in breast cancer cells diminished the levels of extracellular thiols (Figure 2b), eliminated their selenite uptake (Figure 2c), and reduced expression of the selenoprotein antioxidants GPX1 and GPX4 (Figure 2d,e), indicating that Erastin is disrupting xCT-mediated extracellular reduction which leads to selenium uptake and selenoprotein production in these cells. The gene discussed is SLC7A11; the disease is breast carcinoma.