The study of myeloproliferative neoplasms (MPNs) has made substantial progress at the molecular level in the last decade, identifying additional driver mutations associated with over-activated JAK-STAT signaling (MPL515L/K, CALR exon 9); as well as many additional effects on signaling (CBL, LNK); chromosomal modifications (TET2, EZH2, IDH1 IDH2, ASXL-1); RNA shearing (SF3B1, SRSF2, U2AF1) and molecular events of tumor suppressor function (TP53), which together influence the progression and evolution of true erythropoietic (PV), primary thrombocytosis (ET) and myelofibrosis (MF) diseases. Three causative genes have been recognized: JAK2V617F, CALR, and MPL; other genomic and epigenomic abnormalities ASXL-1, EZH, IDH1, IDH2, and SRSF2 mutations are associated with poor prognosis. Three genes JAK2V617F, CALR and MPL were negative and had the worst prognosis. positive CALR gene had the best prognosis. In PV, 99% of patients were positive for JAK2 gene; in ET, 1/2 patients were positive for JAK2 gene, 1/4 patients were positive for CALR gene, and 4% patients were positive for MPL. If myeloproliferative neoplasms (MPNs) are suspected, four genes need to be checked: BCR/ABL, JAK2V617F, CALR and MPL.