Crizotinib-induced molecular remission in RANBP2-ALK–positive JMML. (A) Microscopic appearance of a peripheral blood smear. (B) RANBP2-ALK fusion gene identified by RNA-seq. Data were visualized using the Integrative Genomics Viewer. Brown color indicates reads with exceptionally long (>1000 bp) mate-pair distance in the reference genome (suggesting the presence of chromosomal structural variation). (C) Clinical course of a patient with RANBP2-ALK. Monosomy 7, ALK break-apart fluorescent in situ hybridization (FISH), and RANB2-ALK–specific RT-PCR using RNA extracted from bone marrow or peripheral blood mononuclear cells were monitored over the course of treatment: CET (cytarabine 100 mg/m²/day for 7 days, etoposide 150 mg/m²/day for 3 days, THP-doxorubicin 25 mg/m²/day for 2 days), ECM (etoposide 150 mg/m²/day for 5 days, cytarabine 200 mg/m²/day for 7 days, mitoxantrone 5 mg/m²/day for 5 days; triple intrathecal therapy [methotrexate 12 mg + cytarabine 30 mg + hydrocortisone 25 mg]), and crizotinib 280 mg/m²/day. Open triangle, bone marrow transplantation from matched sibling donor. Preconditioning regimen (busulfan 4.8 mg/kg/day for 4 days, fludarabine 30 mg/m²/day for 4 days, melphalan 90 mg/m²/day for 2 days, anti-thymocyte globulin 1.25 mg/kg/day for 2 days) was administered before bone marrow transplantation.