Whether MPL S505N is a primary pathogenetic event in MPN remains to be elucidated: in vitro studies have shown that this mutation could not induce spontaneous cell growth, tumorigenesis, or spontaneous activation of the main receptor signal transduction pathways [3] whereas computational simulation of a structural model of MPL S505N supports the theory that this mutation can result in constitutive activation of the MPL-JAK2-STAT signalling pathway [15]. This evidence concerns the gene SOAT1 and myeloproliferative neoplasm.