Given that AIM2 ’s activity appears to be intimately linked with SLE pathogenesis (Zhang et al., 2013), the hypomethylation identified at the gene’s promoter by Javierre et al. (2009) provides a plausible mechanism for AIM2 overexpression and suggests that MER41.AIM2 dysregulation might contribute to SLE pathogenesis, at least in some patients. This evidence concerns the gene AIM2 and systemic lupus erythematosus.