Researchers announced development of translational read-through-inducing drugs (TRIDs) capable of bypassing premature stop codons caused by nonsense mutations in Fanconi anemia genes. These small molecules engage the ribosomal machinery to restore synthesis of full-length functional proteins, addressing a fundamental genetic defect underlying this bone marrow failure syndrome. Published in Cell Death Discovery, the study highlights a therapeutic modality that safely enhances translational fidelity without compromising proteome integrity, opening avenues for treating a genetically heterogeneous and difficult bone marrow disease.