Our data also demonstrate that in the absence of ERα signaling, Sle1b is insufficient to induce B cell hyperactivation, suggesting that this phenotype requires the synergistic actions of ERα and Sle1b. Future studies aimed at understanding the basis for this synergy will help to uncover the molecular basis for the ability of ERα signaling to promote loss of tolerance, immune cell activation, and the development of autoimmunity and shed light on the causes of the strong female sex bias associated with these processes. The gene discussed is ESR1; the disease is Autoimmunity.