Although the molecular mechanism underlying the progression of hematopoietic disorders observed in patients bearing PTPN11 mutations is not fully understood, several in vitro and in vivo studies indicate that hyperactivation of the tyrosine phosphatase SHP-2, encoded by PTPN11, may have a role in aberrant activation of both the JAK/STAT and RAS/MAPK/ERK signaling pathways favoring the pathogenesis of NS and JMML.20, 21, 22. The gene discussed is PTPN11; the disease is juvenile myelomonocytic leukemia.