In line with this, receptor–ligand interactions focusing on S100A8 demonstrated downregulation of all S100a8‐Tlr4 mediated interactions of monocytes with monocytes, megakaryocytes, and stromal cells, demonstrating that the S100a8/S100a9‐Tlr4 axis is the most significantly affected pathway in tasquinimod‐treated JAK2V617F MPN associated with fibrosis (Figure 2G). This evidence concerns the gene S100A8 and myeloproliferative disorder.