Downstream products of EGFR might induce phosphorylation of MET, whereas altered c-MET-induced protein may also lead to EGFR phosphorylation.282,287 Activated MET and EGFR might form different heterodimers, resulting in various tumor biological behaviors, such as cell growth and survival for MET-EGFR and MET-HER3 or migration for MET-HER2.288 In addition, MET activation has been observed occasionally in VEGF-targeted therapy, resulting in VEGF resistance; however, the underlying mechanism remains unclear.289,290. Here, MET is linked to neoplasm.