Although we could not directly examine phosphorylation of TSC2 on T1798 reported to be phosphorylated by Pim-2 in myeloma cells [47], that on S939 or T1462, known to be involved in downregulation of its GAP activity [35], became partly resistant to dephosphorylation by the PI3K/Akt inhibitors as well as the FLT3 inhibitor in 32D/TKD cells overexpressing Pim-1, which implies that Pim-1 may upregulate the mTORC1 pathway also at the level of TSC2 directly or indirectly through mechanisms not involving Akt. The gene discussed is AKT1; the disease is plasma cell myeloma.