SLC7A11 and cancer: Initially, it was proposed that SLC7A11‐mediated glutamate export depletes intracellular glutamate and other tricarboxylic acid (TCA) cycle intermediates derived from glutamate, resulting in an increased reliance on glucose‐dependent glycolysis to sustain TCA cycling and mitochondrial oxidative phosphorylation in SLC7A11‐high cancer cells.10, 46