The absence of target mutation and retention of target pathway dependence in our model of acquired rilotumumab resistance is thus unlike many other mechanisms of acquired drug resistance, where mutation of the gene encoding the drug target (e.g., EGFR), loss of prominent negative regulators downstream of the drug target (e.g., PTEN), or activation of alternative mitogenic pathways parallel to the target (e.g., MET in response to EGFR inhibitors) are prevalent means of restoring tumor cell proliferative and invasive activities. This evidence concerns the gene MET and neoplasm.