MET has also been shown to signal synergistically with EGFR as part of a broad signaling network that cooperatively drives activation of these downstream pathways.[22, 40] Indeed, concomitant inhibition of MET and EGFR in erlotinib-resistant cells harboring the T790M mutation significantly increases lung cancer cytotoxicity above MET-targeted therapy alone in both in vitro and in vivo settings.[21]. The gene discussed is MET; the disease is lung carcinoma.