Based on our result, combination of low concentrations of EGFR inhibitors and MEK inhibitors may be clinically relevant in EGFR expressing KRAS wild type pancreatic cancers, which may represent 23% of pancreatic cancers, in addition to the 2% of G12C KRAS mutants who may respond to MEK inhibition alone. The gene discussed is KRAS; the disease is pancreatic neoplasm.