The explanation to this discrepancy is unclear, but an explanation may be observations that K-RAS mutations in tumor cells result in constant activity of EGFR signaling pathways, which might decrease EGFR mRNA by negative feedback due to cross-talk between EGFR activity and K-RAS function as observed in acquired resistance following anti-EGFR treatment of patients[36]. The gene discussed is KRAS; the disease is neoplasm.