NF-kappaB is one of the main transcriptional factors that is responsible for cell survival under stresses. It was shown that various species of mycoplasma and their structural components were able to stimulate NF-kappaB activation as a result of their interaction with specific toll-like receptors on eukaryotic cell surface. Based on these studies, we suggested that activation of NF-kappaB in response to mycoplasmal infection could enhance the resistance of infected cells in response to proapoptotic stimuli. In this study we showed that infection of cells expressing toll-like receptors TLR2/6 with mycoplasma M. arginini leaded to suppression of apoptosis induced by chemotherapeutic agents (cisplatin, 5-fluorouracil, taxol).