Lee et al. found that GPX4 was highly expressed in breast cancer tissues compared with matched normal samples, which was correlated with the increased expression of the xCT subunits SLC7A11; Erastin, an inducer of ferroptosis, depleted levels of the antioxidant selenoproteins GPX4 in breast cancer cells by inhibiting xCT-dependent extracellular reduction, which further demonstrated the synergistic role of SLC7A11/GPX4 in regulating ferroptosis [27]. The gene discussed is GPX4; the disease is breast carcinoma.