Ribosomes are central to cellular growth and proteome maintenance, and cancer cells frequently depend on increased ribosome biogenesis and altered translation to sustain proliferation, stress tolerance, and metabolic rewiring. Paradoxically, inherited “ribosomopathies” caused by germline defects in ribosomal proteins or ribosome biogenesis factors present with tissue hypoplasia and bone marrow failure early in life, yet confer substantially increased lifetime risk of myelodysplastic syndrome (MD