Inhibition of the kinase domain of EGFR and the resultant oncogenic cell signaling disruption by small molecule inhibitors have been shown to be particularly beneficial in patients carrying the so-called “sensitizing mutations” such as L858R and the exon-19 deletion [1, 2], which contribute to nearly 90% of lung-cancer-specific EGFR mutations [3, 4]. The gene discussed is EGFR; the disease is lung carcinoma.