This result supports the suggestion that other MEK–ERK-independent signaling pathways (likely those regulated by PI3K–AKT discussed above) also contribute to apoptosis induced by gefitinib in NSCLC harboring activating mutations of EGFR. More generally, these data reveal important differences between the signaling pathways triggered by EGFR kinase inhibitors and those induced by antagonistic monoclonal antibodies, and present a rational means for improving clinical responses to cetuximab - by combining it with MEK inhibitors. Here, MAP2K7 is linked to non-small cell lung carcinoma.