To analyze how pathophysiologically relevant EGFR mutations perturb the signaling network, we profiled EGF signaling activity in lung cancer metastases-derived H838 cells expressing the wild-type EGFR and compared the results to H838 cells harboring the exogenously expressed EGFR that carries the activating mutation L858R and the resistance mutation T790M (H838-EGFRmut). This evidence concerns the gene EGF and lung carcinoma.