U2AF1 and myelodysplastic syndrome: Similarly, Alper et al. (77–79) showed that inhibition of spliceosome genes reduces inflammatory cytokine production in response to TLR agonists, and conversely, expression of MDS-associated spliceosome mutations (involving splicing factors U2AF1, SF3B1, or SRSF2) enhances NF-κB activity and cytokine production by K562 myeloid leukemia cells following TLR stimulation.