Fig. 2From: Impact of MET alterations on targeted therapy with EGFR-tyrosine kinase inhibitors for EGFR-mutant lung cancerMET amplification causes EGFR-TKI resistance by activating EGFR-independent phosphorylation of ErbB3 and consequent downstream activation of the PI3K/AKT pathway, providing a resistance mechanism that can bypass the effects of an EGFR-TKI. MET can also activate PI3K/Akt signaling through ErbB3Back to article page