However, when we carried out similar assays with a SuperSelective primer designed to detect the single-nucleotide polymorphism in the EGFR L858R mutant sequence, whose presence in non-small-cell lung cancer predicts resistance to tyrosine kinase inhibitors [24, 25], we found that its presence in a G-C rich wild-type sequence (3'-ACCCGAC-5') resulted in less suppression of wild-type amplicon synthesis. This evidence concerns the gene EGFR and non-small cell lung carcinoma.