The aberrantly spliced genes identified in SF3B1, SRSF2, and U2AF1 mutant MDS were shown to converge in common dysregulated cellular processes and pathways, focused on RNA splicing, protein synthesis, and mitochondrial dysfunction, suggesting common mechanisms of action (Fig. 1).8▪ Several dysregulated pathways and cellular processes could be linked to MDS pathophysiology, while others, such as sirtuin signaling, represented new players. The gene discussed is U2AF1; the disease is myelodysplastic syndrome.