Previous evidence has shown that dysregulated ferroptosis-related genes play an important role in revealing intertumoral immune heterogeneity and indicate potential clinical benefits for anti–PD-1/PD-L1 immunotherapy in lung adenocarcinoma.32 Additionally, Zhou et al32 reported that TYRO3 inhibited tumor cell ferroptosis triggered by anti-PD-1/PD-L1 and facilitated the development of a protumor microenvironment by reducing the M1/M2 macrophage ratio, resulting in resistance to anti-PD-1/PD-L1 therapy. Here, CD274 is linked to lung adenocarcinoma.