SLC7A11 and cancer: The main regulatory pathways involved in disulfidptosis are the cystine uptake and glucose metabolism pathways, of which SLC7A11 is a key factor.[9] Further studies are needed to determine whether the hypersensitivity to glucose transporter protein inhibition observed in tumors with high SLC7A11 involves other mechanisms.[30] In addition, further exploration and validation of disulfidptosis-targeting strategies in both preclinical and clinical settings may usher in a new era of precision medicine for SLC7A11-high cancers or other related diseases.[30,31]