Multiple mechanisms of acquired resistance to TKIs have been identified, including secondary EGFR mutation in threonine 790 (T790M), MET amplification, human epidermal growth factor receptor2 (HER2) amplification, conversion from NSCLC into small cell lung cancer, and loss of phosphatase and tensin homolog (PTEN) [8]. This evidence concerns the gene EGFR and non-small cell lung carcinoma.