EGFR and non-small cell lung carcinoma: The latter scenario is more common than the selection of preexisting drug resistant subclones, a phenomenon known as acquired resistance.6,7 Although the mechanisms of TKI acquired resistance, such as secondary mutations within the EGFR allele, alterations of other RTKs or downstream effectors, bypass signaling activation, and phenotypic transformation,7 have been well established, the acquired resistance occurs in about one third of NSCLC without any of these alterations.8