Beyond FAP, signaling pathways such as Galectin-1 (Gal-1), the fibroblast growth factor receptor (FGFR)-Gremlin-1 axis, and glucocorticoid (GR) receptor signaling have emerged as key mediators of tumor–stroma crosstalk, particularly in treatment-resistant disease [21–24]. This evidence concerns the gene FAP and neoplasm.