The differential interactome composition indicates a functional shift in EGFR signaling that may drive increased tumor cell adhesion (CD44, ITGB1, FN1), metabolic adaptation (GAPDH, ENO1) and stress response (HSPA4, HSP90AB1), consistent with mechanisms observed in therapy‐resistant CRC phenotypes [15]. This evidence concerns the gene FN1 and colorectal carcinoma.