JPM-OEt (50 mg/kg; i.p.; daily for 30 days) decreases tumor cathepsin B activity obviously[1]. JPM-OEt (50 mg/kg; i.p.; twice daily for 4 weeks) causes tumor regression in the RIP1-Tag2 (RT2) mouse model of pancreatic islet cell tumorigenesis[2]. JPM-OEt (50 mg/kg; i.p.; daily from 63 to 98 days) leads to an obviously delay in the increase of tumor burden during the first 2 weeks of treatment[3].