AP1S1 was also elevated, though with more modest survival associations; it regulates EGFR trafficking in NSCLC, and its perturbation promotes lysosomal EGFR degradation and alters TKI response, while literature links STAT3 activity to oxidative phosphorylation and therapy resistance, supporting an immune-metabolic interpretation 82, 83. Here, AP1S1 is linked to non-small cell lung carcinoma.