This is attributed to cross-phosphorylation between EGFRvIII and wild-type EGFR, amplifying oncogenic signaling cascades.137 Notably, EGFRvIII expression is correlated with increased tumor heterogeneity, complicating treatment responses and limiting the efficacy of targeted therapies, including tyrosine kinase inhibitors and immunotherapy.138. The gene discussed is EGFR; the disease is neoplasm.