The transcription factor Ets1 plays a critical role in maintaining B cell quiescence. High levels of Ets1 expression in resting B cells prevent premature plasma cell differentiation and autoimmune responses, but it must be downregulated in response to antigen receptor stimulation to allow for proper B cell responses. Despite its vital function, it remains unknown how this Ets1 expression pattern is coordinated. The goals of this project are to identify the transcription factors and regulatory elements involved in maintaining Ets1 expression in the resting B cell, and to parse out the signaling pathways and downstream effectors required for downregulating Ets1 in response to antigen receptor stimulation.