This approach uses a lentiviral MSCV-IRES-eGFP (MIG) vector to overexpress wild-type SAMD9, SAMD9L, or mutations that we have previously identified in children with MDS (SAMD9: E1136Q; SAMD9L: H880Q, W1180R, or R1281K) [3, 4]. This evidence concerns the gene SAMD9 and myelodysplastic syndrome.