To the Editor Juvenile myelomonocytic leukemia (JMML) is an aggressive myeloproliferative neoplasm of childhood with nearly half of all patients relapsing within 3 years [1,2]. More than 90% of JMML patients present with initiating mutations in NF1, KRAS, NRAS, RRAS, RRAS2, CBL, and PTPN11, all leading to hyperactivation of the Ras pathway [3]. Patients with additional molecular alterations including cytogenetic abnormalities, and in particular, point mutations in SETBP1 have inferior outcomes [4]. At present, hematopoietic stem cell transplantation (HSCT) is the only curative therapy, with the primary cause of death being relapse or progression to acute myeloid leukemia (AML) [5]. Recently, JMML patients who did not display Ras pathway mutations were found to have ALK and ROS1 fusions that were sensitive to ALK inhibition [6]. Given the poor overall survival of JMML patients even after intensive treatments such as HSCT, opportunities to implement precision medicine should be