One potentially confounding factor is that the treatments that this cohort of patients underwent prior to investigation of EphB4 protein expression in their tissues is not fully known; therefore, an alternative explanation for our findings is that those who were treated with chemotherapy regimens or even small-molecule tyrosine kinase inhibition (TKI), neither of which are 100% specific to a single molecular target within tumor cells, survived longer simply because they expressed EphB4 and therefore EphB4 activity was partially being abrogated. This evidence concerns the gene EPHB4 and neoplasm.