David Ross Camidge, MD, PhD of the University of Colorado, Denver, CO, provides an insight into emibetuzumab, a monoclonal antibody directed towards the mesenchymal-to-epithelial transition (MET) factor. MET can be a primary driver of some subtypes of lung cancer, particularly the mutated MET Exon 14, and highly amplified versions of MET. He further explains that it is also a mechanism of acquired resistance in those who have an EG5 mutation, who were initially treated with an Eg5 kinesin inhibitor, but then develop acquired resistance. He explains that we already understand T790M mutation, which occurs in about 60% of cases. He elaborates in saying that in this study (NCT01631552), patients were enriched in having the EG5 mutation. Patients were not formally tested up front, and instead, the Jackman criteria was used, deriving clinical benefit. When patients developed acquired resistance, patients were enriched in those who may have had MET as their mechanism of action. This enrichment looked at MET expression by immunohistochemistry. Prof. Camidge explains that in the study, whether you got emibetuzumab alone, or emibetuzumab and kept the EGFR tyrosine kinase inhibitor (TKI) going on, the response rate was very low, and there did not appear to be a difference in the progression-free survival (PFS). This tells us that we are not identifying the right population yet, both because we did not just do the EG5 mutation, and secondly because the enrichment methods driven by MET in an acquired resistance setting did not have a bar that was set high enough. Therefore, he believes that we could approach the concept again, and look at patients who were super-high expressers of MET, and then look at other methods looking at MET activation as acquired resistance. Recorded at the 2016 Annual Meeting of the American Society of Clinical Oncology (ASCO), held in Chicago, IL.