Activating mutations in KRAS or NRAS constitutively activate the mitogen‐activated protein kinase (MAPK) pathway, similarly driven by BRAF V600E, bypassing EGFR inhibition.[129, 130, 131, 132] Activating mutations in PIK3CA sustain AKT signaling despite EGFR blockade.[133] 2) EGFR structural modifications, EGFR extracellular domain mutations (e.g., S492R) preventing antibody binding,[134] and cetuximab could bind to truncated EGFRvIII but did not modulate the proliferation or radiosensitivity of EGFR vIII‐expressing cancer cells.[135] 3) Activation of compensatory RTKs. The gene discussed is KRAS; the disease is cancer.