Tumor necrosis factor-alpha (TNF-${alpha}$) is a proinflammatory cytokine that mediates the inflammatory response and immune functions, and modulates the proliferation, differentiation and cell death of cancer cells. The differential functions of TNF-${alpha}$ in various human cells due to the formation of different stimulating pathway upon the binding of TNF-${alpha}$ to its receptors. In the present study, we examined the different effects of TNF-${alpha}$ on the survival and apoptosis between normal granulocytes and human myeloid leukemia HL-60 cells. Although TNF-${alpha}$ did not affect on the constitutive apoptosis of granulocytes, TNF-${alpha}$ strongly induced the apoptosis of HL-60 cells in a dose- and a time-dependent manner. TNF-${alpha}$-induced apoptosis was occurred via the activation of caspase 8, caspase 9 and caspase 3/7 and the induction of ROS production in HL-60 cells. Also, BAY-11-7085, a NF-${kappa}B$ inhibitor, blocked the TNF-${alpha}$-induced apoptosis in HL-60 cells. NF-${kappa}B$ may be involved in TNF-${alpha}$-induced apoptotic signaling pathway in HL-60 cells. These results suggest that TNF-${alpha}$ activates apoptotic pathways and its process depends on cell type and many cellular factors. A better understanding of the differential effect of TNF-${alpha}$ on cell apoptosis and survival may provide important information that can be used to elucidate the specific inhibitory effect of TNF-${alpha}$ on the cancer dis.