Knock-down of Socs2 caused a decrease of immunophenotypically defined LSCe among Venus+ RFP+ LCs (Fig. 5F), lessened the number of quiescent LSCe (Fig. 5G), and reduced clonogenicity in a serial replating assay (Fig. 5H), indicating that Socs2 enhanced LSC abundance and function in the MLL-AF9 mouse model of AML. Here, SOCS2 is linked to acute myeloid leukemia.