While upregulation of BCL2 was noted in MDS/AML clones that escaped IRAK1 inhibitor treatment, synergistic reduction of cell expansion and viability was obtained upon the addition of BCL2 inhibitor to an IRAK1 inhibitor suggesting that there is synergy between TLR signaling blockade and inhibition of anti-apoptotic pathways in myeloid malignancies (94). This evidence concerns the gene IRAK1 and myelodysplastic syndrome.