The SAMD9 and SAMD9L mutations identified in pediatric MDS and AML encode biochemical gain-of-function proteins that inhibit Ras/mitogen-activated protein kinase (MAPK) signaling, suppress cell growth, perturb protein translation, and promote apoptosis, which favors the survival of Mo7/del(7q) clones that delete the mutant allele [3, 16, 17]. This evidence concerns the gene SAMD9L and myelodysplastic syndrome.