Introduction: Acute myeloid leukaemia (AML) is a clonal haematological neoplasm characterised by proliferation of immature myeloid cells in the bone marrow resulting in impairment normal cell development in bone marrow. This leads to anaemia, thrombocytopenia and neutropenia. AML primarily affects older adults, with a median age at diagnosis of 69 years but is also seen in all other age groups. AML is recognized as a kind of cancer with marked heterogeneity in both biology of the cells and reactions to treatment. Treatment with intensive chemotherapy regi-mens of adult AML patients who are ≤ 60 years old results in hematologic remission in about 35% of patients, but at least 30% of these patients will experience a relapse. Mechanism leading to early relapse is still unclear. Leukaemia stem cell (LSC) is shown to correlate with poor prognosis. Biomarkers such as aldehyde dehydrogenase (ALDH) and CD34+CD38- have been identified as potential LSC biomarkers in previous studies. The objective of this study is to examine the expression of such markers for LSC and determine the association. Methods: Peripheral blood or bone marrow samples from untreated, newly diagnosed acute myeloid leukemias of all age, gender and race were collect-ed from Hospital Melaka and Kelang. Diagnosis of AML is based on WHO classification which include morphology, cytochemistry, immunophenotyping and cytogenetics. Mononuclear cells were isolated from bone marrow aspirate samples by gradient density centrifugation on Ficoll-Hypaque. Immunophenotyping using CD13, CD14, CD33, CD34, CD38 and ALDH were carried out to identify the presence and proportion of the various populations of inter-est. Results: There was a strong, positive correlation between ALDH and CD34+CD38- cell population, which was statistically significant (rs = 0.5989, p< 0.05). Conclusion: The strong correlation of ALDH activity and CD34+CD38- expression supported the potential of these biomarkers to identify LSCs cell in AML patients. However, due to the heterogeneity of AML, further studies using more markers and larger sample size are needed to determine the validity and to correlate with disease-free survival rate of AML patients.