Increasing evidence from our lab and others supports that ribosomal proteins play a critical role in development1 and diseases including bone marrow disease 2 in addition to its essential role in protein synthesis. We found Rpl22 is dispensable for protein biosynthesis but regulates transformation and hematopoiesis 1, 3. Previously I have determined that Rpl22 functions as a haploinsufficient tumor suppressor in a mouse T-cell lymphoma model by activating NFB and its target Lin28B 3. Recently we also found that Rpl22 knockout mice exhibit an MDS-like phenotype associated with anemia and abnormal bone marrow BM hematopoiesis. Consistent with what we observed in our mouse model, our collaborator found that Rpl22 was mutated or deleted in some MDS and AML patients.