Previously, we have demonstrated that SLC7A11 promotes glucose dependency, and high expression of SLC7A11 is a major contributor to triggering disulfidptosis in tumor cells.[6] To further study the mechanistic regulation of disulfidptosis by SLC7A11, we assessed the expression levels of SLC7A11 in several human cancer cell lines (Figure S1A, Supporting Information). This evidence concerns the gene SLC7A11 and neoplasm.