BTG3 and systemic lupus erythematosus: Indeed, a higher relative prevalence of genetic forms of SLE (recently estimated to be ∼7% [21]) and a higher number of risk alleles within individuals across the remaining JSLE patient population [22] likely contribute to more severe clinical phenotypes with increased disease activity and organ damage, and higher proportions of ANA-negative patients when compared with adult-onset SLE [23].