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remains somewhat limited.Here, we report our experience at a tertiary care academic medical center, with a newly implemented inhouse myeloid specific panel, in terms of diagnostic yield, molecular spectrum and appropriateness of test utilization.Methods: Among the cases that completed the Oncomine Myeloid Assay (OMA), 281consecutive cases runs were analyzed.DNA from bone marrow or peripheral blood was sequenced at >200 mean depth.Variants were classified according to the ACMG/AMP guidelines.Diagnostic yield was defined as detection of 1 pathogenic or likely pathogenic (P/LP) variant.The clinical impact and appropriateness of testing were assessed for each case based on clinical findings.Results: A total of 281 cases were divided into five groups based on their clinical presentation: persistent cytosis (n=63), unexplained cytopenia (n=83), suspected lymphoid disorders (n=18), suspected myeloid neoplasm (n=104), and other diagnoses, including solid tumors (n=13).Pathogenic or likely pathogenic variants were identified in 45% of all cases (127/281), with the number of variants per case ranging from one to eight.Diagnostic yields across the five subgroups were 25.3% (16/63), 33.7% (28/83), 44.4% (8/18), 70.2% (73/104), and 15.4% (2/13), respectively.Among the positive cases, 89.2% (118/ 127) carried clinically relevant variants, defined as those with diagnostic, prognostic, or therapeutic significance.The most frequently mutated genes were TET2 (35.7%),ASXL1 and DNMT3A (22.2% each), JAK2 (19%), SRSF2 and PHF6 (11.1% each), NRAS, FLT3, TP53 and IDH1 (~10% each).Among the 55% (154/281) of cases with negative results, around 20% (31/154) had documented clinical suspicion of myeloid neoplasm, whereas 30.5% (47/154) and 35.7% (55/154) were ordered due to persistent cytosis and unexplained cytopenia, respectively.Among the 29 cases diagnosed with myeloid neoplasms (10.3%, 29/281), repeat NGS testing on subsequent samples revealed DDX41mutation gain, FLT3-ITD clonal complexity, stable TET2 clones, and GATA2 clonal loss.These findings reflect significant clonal shifts and potential molecular responses that may significantly influence therapeutic management, predict relapse risk, and identify clonal persistence in residual disease. Conclusion:The OMA myeloid panel demonstrates high diagnostic yield and meaningful clinical impact when used appropriately.Serial molecular monitoring aids in detecting clonal shifts and emerging resistance.The high percentage of negative results may reflect suboptimal test utilization, highlighting the importance of pretest screening in optimizing molecular testing in myeloid disorders.