Further, they showed that S100A9- induced signaling activates NADPH oxidase, increasing ROS and triggering pyroptosis and β-catenin activation in MDS BM-MNCs, and inhibition of S100A9 using a decoy receptor reduced transcriptional priming of pyroptosis-associated genes (CASP1, IL-1B, IL-18, and NLRP3) and improved the colony-forming capacity of BM-MNCs from patients with MDS. This evidence concerns the gene FMO5 and myelodysplastic syndrome.