In acute myeloid leukaemia (AML), cell kinetic quiescence has been postulated to contribute to drug resistance. As the anti‐apoptotic genes Bcl‐2 and Bcl‐X_L have been implicated in cell cycle regulation, we investigated the expression of these genes in non‐proliferating (Q) and proliferating (P) AML and normal CD34⁺ progenitor cells. Using reverse transcription polymerase chain reaction, Bcl‐X_L and Bcl‐2 were overexpressed in Q versus P AML cells, whereas no difference in Bcl‐X_S and Bax expression was found. Furthermore, the Bcl‐X_L/X_S but not the Bcl‐2/Bax ratio was higher in Q AML compared with normal CD34⁺ Q cells (P = 0·001). An inverse correlation between Bcl‐2 expression of leukaemic Q cells and their ability to enter the cell cycle was found. Treatment with all‐trans retinoic acid (ATRA) reduced Bcl‐2 and Bcl‐X_L expression in the leukaemic Q cells, and enhanced their chemosensitivity to cytosine arabinoside (ara‐C). These findings demonstrate overexpression of the anti‐apoptotic proteins Bcl‐X_L and Bcl‐2 in quiescent CD34⁺ AML cells and suggest their involvement in the chemoresistance. The observed inverse correlation between Bcl‐2 and proliferation suggests a role for Bcl‐2 in the cell cycle regulation of AML. These findings could be used in the development of therapies that selectively induce apoptosis in quiescent leukaemic progenitor cells.