Although these results are because of the lack of patient cohorts treated by METi rather of a descriptive nature, the correlations demonstrate that the MET-E2F1-purine synthesis cascade is frequently altered in human cancer, and one of the tasks of the upcoming clinical trials should be to elucidate the role of this axis in responses to anti-MET targeted-monotherapies and combined treatment regimens. The gene discussed is MET; the disease is cancer.