In NSCLC models, SH003 ± docetaxel suppresses the EGFR–JAK–STAT3 axis and yields synergistic antitumor activity; accordingly, exosome-based metabolomic signatures in this setting are best positioned as exploratory predictive biomarkers rather than mechanistic effectors, pending prospective immune-functional validation [6,99,102,103,104,105]. This evidence concerns the gene STAT3 and non-small cell lung carcinoma.