Further investigation demonstrated that the highest response rates to these TKIs were seen in patients with somatic mutations within the EGFR-TK domain, particularly exon 19 deletion, exon 21 L858R, and exon 18 G719X.[5]
By contrast, the exon 20 T790M mutation is associated with acquired resistance to TKI therapy.[6]
http://emedicine.medscape.com/article/1689988-overview