Transcriptional profiling also revealed other dysregulated immune cell types in MDS, including non-classical monocytes, characterized by elevated expression of inflammatory markers such as ADORA2A and the alarmin S100A8. A recent preclinical study demonstrated that S100A9, secreted by monocytes/macrophages and forming a heterodimer with S100A8, can drive inflammatory activation of stromal cells and impair hematopoietic function in MDS134. This evidence concerns the gene ADORA2A and myelodysplastic syndrome.