The study found that more than 50% of MDS patients had overexpression of TLR signaling pathway and downstream effector molecules, including TLR-1, TLR-2, TLR-4, TLR-6, TLR-7, TLR-9 and its downstream effector molecules such as MyD88 or IRAK1 and IRAK4 kinases (66, 67). This evidence concerns the gene MYD88 and myelodysplastic syndrome.