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The leucine-to-arginine substitution at residue 858 (L858R) and in-frame exon 19 deletion make up about 90% of EGFR activating mutations and cause higher binding affinity of the ATP-binding site of EGFR to tyrosine kinase inhibitors (TKIs), thereby increasing the vulnerability of EGFR to inhibition of its kinase activity [1, 2]

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The source doesn't matteronly particle concentration