Interestingly, the SF3B1 K700E mutation promotes alternative splicing of Interleukin-1 receptor-associated kinase 4 (IRAK4) to generate a long isoform (IRAK4-L) in MDS and AML, which interacts with MyD88 to elicit hyperactivation of NF-κB and leukemogenesis [10,38]. The gene discussed is NFKB1; the disease is myelodysplastic syndrome.