Typically, it was demonstrated that CD8+ T cells activated by immunotherapy could release IFNγ to inhibit the expression of SLC7A11 in tumor cells and impair the cystine uptake, thus inducing tumor cell ferroptosis.[128] Extending from the interaction between ferroptosis and immunotherapy, the authors designed an engineered cystine‐degrading enzyme called cyst(e)inase, which could synergize with PD‐L1 immunotherapy for enhanced tumor inhibition efficacy. This evidence concerns the gene SLC7A11 and neoplasm.