In addition, recent studies showed the pharmacogenomic issues in EGFR determine the limitation of gefitinib in clinical applications: Activating mutations of the in-frame deletions (ΔE746-A750) in exon 19 and the L858R point mutation in exon 21 of the EGFR tyrosine kinase domain in NSCLC are highly correlated with gefitinib sensitivity [11], [12], [13]. The gene discussed is EGFR; the disease is non-small cell lung carcinoma.