Aberrantly spliced genes and dysregulated pathways were also identified in bone marrow erythroid and myeloid precursors of SF-mutant MDS patients.8▪ Emerging data from recent studies showed that SF3B1, SRSF2, and U2AF1 mutations result in hyperactive NF-κB signaling via aberrant splicing of MAP3K7, CASP8, and IRAK4, respectively.10▪,11. Here, U2AF1 is linked to myelodysplastic syndrome.