Indirect evidence from our experiments suggests that JAK/STAT signaling (specifically STAT3) could be pertinent in the regulation of S100A8 expression, whereas discrepant epigenetic changes could be the key to the divergent S100A8 levels between type 1 and type 2 CALR-mutated MPN cells. This evidence concerns the gene S100A8 and myeloproliferative neoplasm.