Emphasizing the importance of epistatic effects in the development of SLE, the combination of a Fcgr2b deficiency and a Dnase1l3 deficiency was shown to result in enhanced SLE-like disease in comparison to the individual knockouts, as for example the serum levels of dsDNA autoantibodies increased by a factor of 40 (22). The gene discussed is FCGR2B; the disease is systemic lupus erythematosus.