The authors attributed this striking phenotype to the function of MSI2 in maintaining the LIC self-renewal gene expression program by targeting leukemogenic MLL target transcripts Hoxa9, Myc, and Ikzf2. The Kharas group subsequently determined that depletion of SYNCRIP, a novel MSI2 interacting protein resulted in increased apoptosis, decreased proliferation, and increased differentiation in human MLL-AF9 AML cell lines and inhibited leukemia progression in an in vivo murine model [138]. The gene discussed is MYC; the disease is acute myeloid leukemia.