Multiple studies have suggested different mechanisms that can explain this variability and the generation of tumor resistance: EGFR polymorphisms and mutations(e.g., EGFR G465R)10,11; overexpression of activated receptor downstream tyrosine kinases involved in the EGFR pathway12; or downregulation of EGFR pathway inhibitory intermediates (e.g. DUSP5, DUSP6)13. This evidence concerns the gene EGFR and neoplasm.