Reactive oxygen species play a role in signal transduction and in many human diseases. B-cell activating factor (BAFF) plays a role for mature B cell generation and maintenance and for the incidence of autoimmune diseases. We previously reported that BAFF expression was induced by ROS. In this study, we investigated whether ROS-induced BAFF expression was affected by toll-like receptor (TLR) 4 or myeloid differentiation primary response gene (MyD) 88. BAFF expression was increased by serum deprivation that is an experimental modification to produce ROS. In contrast, TLR4 and MyD88 were decreased by serum deprivation. Although ROS production was decreased in TLR4-nonfunctional or MyD88-deficient splenocytes as compared to that in control mice, serum deprivation increased ROS production and augmented BAFF expression in both cells. $50{mu}M;H_2O_2$ also increased BAFF expression in TLR4-deficient or MyD88-deficient splenocytes. Collectively, results show that BAFF expression may be mediated by TLR4 or MyD88-independent manner and TLR4 or MyD88 may not be required in BAFF expression.