One explanation of the persistent survival of lung cancer cells to EGFR inhibition is that while these inhibitors initially suppress MEK/ERK and AKT activity downstream of EGFR signaling, the suppression of AKT decreases the transactivation function of the ETS-1 transcription factor, leading to suppression of expression of dual-specificity phosphatases (DUSPs) [91–94] which negatively regulate ERK activity [95, 96]. This evidence concerns the gene EGFR and lung carcinoma.