Mechanistically, anti-PD-1/PD-L1 treatment can significantly increase the expression of TYRO3 in breast cancer tissues, further elevate intracellular Nrf2 levels, reduce ROS generation, inhibit ferroptosis, create a tumor-promoting microenvironment, and confer resistance to anti-PD-1/PD-L1 therapy. The gene discussed is NFE2L2; the disease is neoplasm.