In agreement, multiple reports have shown partial responses of patients harboring A763_Y764insFQEA insertions to the first-generation inhibitor erlotinib, indicating that these mutations may behave similarly to classical NSCLC EGFR mutations.19,48 An outstanding question is whether the downstream signaling pathways activated by distinct EGFR exon 20 insertion mutations are the same and to what degree these pathways overlap with those activated by the more common L858R or exon 19 deletion EGFR mutations. This evidence concerns the gene EGFR and non-small cell lung carcinoma.