Due to the prevalence of mutations in spliceosomal proteins, such as DDX41, SF3B1, U2AF1, or SRSF2 in AML/MDS patients, it is tempting to speculate that DHX34 mutations and/or alternative splicing changes found in these patients could compromise not only its function in NMD, but also affect splicing events mediated by DHX34. This evidence concerns the gene DHX34 and myelodysplastic syndrome.