Pinning down myeloma with Pim2 inhibitors!

Abstract

In this issue of Blood, Lu et al shed light on the role of proviral integration sites of Moloney 2 (Pim2) kinase in multiple myeloma and delineate the mechanisms by which it mediates clonal plasma cells proliferation. The authors identify the tumor suppressor tuberous sclerosis 2TSC2 as the direct phosphorylation substrate of Pim2, suppressing its GTPase activity toward the small G-protein Rheb within the mammalian target of rapamycin C1 (mTORC1) complex. Based on this work, Pim2 inhibitors may indeed be the missing "torc" that pins down myeloma cells proliferation.