Intriguingly, heterozygous female mice, which have Nox2-deficiency in 50% of neutrophils on average due to X-chromosome inactivation, also developed exacerbated lupus and altered autoantibody patterns, suggesting that failure to undergo normal Nox2-dependent cell death may result in release of immunogenic self-constituents that stimulate lupus [102]. Here, CYBB is linked to systemic lupus erythematosus.