The utilization of PD-L1 blockers elicits the secretion of IFN-γ by CD8+T cells, leading to the inhibition of transcription and expression of SLC7A11 and SLC3A2, thereby reducing GPX4 production via the JAK1/STAT1 pathway and facilitating ferroptosis in tumor cells [34]. Here, STAT1 is linked to neoplasm.