We have proved in vitro and in vivo on a mouse xenograft model of MCL that treatment of patients, who progress on or relapse after high-dose araC-based regimen should not rely on nucleoside analogs, namely on the currently used agents fludarabine, gemcitabine and cladribine, since all of them must be phosphorylated by DCK to exert their anti-lymphoma activity. The gene discussed is DCK; the disease is mantle cell lymphoma.