Our analysis would suggest a role for hypermethylation in the regulation of PLC-beta3, at least in CMML leading to constitutive activation of STAT5 similar to what is observed in CML and other MPN associated with the BCR-ABL1 oncoprotein [44] or mutations of JAK2 gene [45]. The gene discussed is ABL1; the disease is myeloproliferative neoplasm.