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]. The gene discussed is GAPDH; the disease is colorectal carcinoma.