Finally, complementary genetic and biochemical studies have shown that the T-ALL-associated uL16-R98S missense mutant disrupts Nmd3 release, thereby blocking the access of Sdo1 to the P-site that in turn reduces Efl1 binding and the subsequent removal of eIF6 (Patchett et al., 2017). The gene discussed is NMD3; the disease is acute lymphoblastic leukemia.