In many MDS cases, TLR signaling is severely overactive due to the overexpression of activators (e.g., myeloid differentiation primary response 88, TIR Domain Containing Adaptor Protein, interleukin-1 receptor-associated kinase 4, and Tumor necrosis factor receptor-associated factor) and downregulation of repressors (e.g., miR145 and miR146a). This evidence concerns the gene IRAK4 and myelodysplastic syndrome.