A novel class of translational read-through-inducing drugs (TRIDs) has been developed to address nonsense mutations in Fanconi anemia, a genetic disorder causing bone marrow failure and cancer susceptibility. These compounds enhance ribosomes' ability to bypass premature stop codons during mRNA translation, restoring production of full-length functional proteins essential for DNA repair. Rigorous biochemical and pharmacological innovation ensures selective modulation of translational fidelity, avoiding deleterious alterations. The study, published in Cell Death Discovery, marks a significant advance toward molecularly targeted therapies for genetically heterogeneous Fanconi anemia patients.