Indeed, the present results lead us to hypothesize that the low uptake in the GL261 tumor model is most likely primarily due to a blood-brain-barrier (BBB) defect and not to specific binding to PSMA for the following reasons: First and foremost, the competitive binding assay indicated that the tumor signal in blocked mice is higher than the uptake in unblocked mice (Figure 6). The gene discussed is FOLH1; the disease is neoplasm.