These findings were then validated by treatment of primary MDS BM-MNCs with RU.521, which suppressed inflammasome activity as evidenced by a reduction in caspase-1 cleavage, IL-1β maturation, and generation of adaptor protein apoptosis-associated speck-like protein containing CARD (ASC) specks, a reliable surrogate for inflammasome activity (24) (Figure 4, A and B). This evidence concerns the gene IL1B and myelodysplastic syndrome.