Induction of apoptosis or differentiation are two promising cancer prevention and therapy strategies. For this purpose, human myeloid leukemia (HL60) cells have been used as a model for studying apoptosis and cell differentiation induction. We have previously shown that the flavonoid apigenin caused apoptosis of HL60 cells. The aim of this work was to evaluate the effect of apigenin in the expression of Bcl2 protein and of tumoral necrosis factor receptor 1 (TNRF1), as well as the cellular redox status. For this purpose, HL60 cells were treated with apigenin (20, 30 µM and 40µM), for 24h. We observed that apigenin caused downregulation of Bcl2 protein and TNFR1, responsible for anti- and pro-apoptotic responses, respectively. Interestingly, the thiol concentration and glutathione reductase activity were not affected after the treatment of HL60 cells with apigenin, for 24h. Our results suggest that the HL60 cells apoptosis induction by apigenin was not dependent on TNFR1, and that apigenin has a strong potential as an agent for preventing leukemia.