## 3 Discussion  
The discovery and implementation of targeted cancer-directed therapy has thrust the field of oncology forward and improved survival for patients with various malignancies. In the treatment of AML, this has been best demonstrated by treatment of patients with FMS-like tyrosine kinase 3 internal tandem duplication (_FLT3_-ITD), an alteration present in about 30% of adult AML patients and 15% of pediatric AML patients. _FLT3_-ITD confers an especially poor prognosis with a high likelihood of relapse even after allogeneic stem cell transplant. However, the addition of TKIs that target FLT3, such as sorafenibb, midostaurin, or gilteritinib, into frontline treatment in combination with conventional chemotherapy has reduced relapse rates and improved survival [16; 17]. With this success, which is thought to be related to improved disease control before transplant, clinical practice has shifted toward also including a FLT3-targeting TKI as post-transplant maintenance therapy with the goal of reducing post-transplant relapses. While there is not yet a clear best practice or guideline for utilizing TKIs as post-transplant maintenance therapy in patients with _FLT3_-ITD+AML, many studies have shown survival benefits with tolerable toxicity profiles and costs [18]. The current Children's Oncology Group frontline AML study, AAML1831, includes TKI (gilteritinib) maintenance therapy for one year after HSCT for patients with _FLT3_-ITD+AML.  
Using this rationale, we hypothesized that adding the ALK-targeting TKI crzotinib to frontline treatment _and_ as post-transplant maintenance therapy would benefit our patient. During upfront therapy, crizotinib was well tolerated and potentially contributed to the patient achieving and maintaining MRD negativity prior to HSCT. Unfortunately, because of the rarity of \(ALK\) fusions in AML, there are no existing prospective trial data to support prophylactic post-HSCT maintenance therapy in a MRD negative state for AML with \(ALK\) fusions, which has led to roadblocks in achieving insurance coverage of the medication.  
In summary, this case study draws attention to a rare but targetable oncogenic fusion in a patient with AML, and it is the first reported case of an \(ALK\) fusion in AML _without_ monosomy 7. Most institutional AML FISH probe sets do not include \(ALK\); thus, we must rely on DNA and RNA sequencing as a crucial diagnostic tool to identify these and other rare, potentially actionable gene alterations. Our case study also highlights the challenges of our third-party payor health care system, which have substantial impact on physicians' ability to use relevant, albeit limited, data to offer targeted agents off-label to patients with rare conditions.  
Conceptualization, M.S.R. and M.S.; writing--original draft preparation, M.S. and G.L.C.; writing--review and editing, M.S.R.; visualization and formal analysis, J.N.P., C.V.C. and K.E.F. All authors have read and agreed to the published version of the manuscript.  
This report received no external funding.  
This case study was conducted according to the guidelines of the Declaration of Helsinki and approved by the Institutional Review Board of Baylor College of Medicine/Texas Children's Hospital H-51145, approved on 15 February 2022.  
Informed Consent Statement: Informed consent was obtained from all subjects involved in the study.  
No new data were created or analyzed in this study. Data sharing is not applicable to this article.  
We would like to thank all those involved in the clinical care of this patient, as well as all laboratory staff who were involved in generating and reporting the results that allowed us to best treat this patient.  
The authors declare no conflict of interest.