IFNA1 and systemic lupus erythematosus: Although it was recently reported that anti-DNA autoreactivity was driven by type I IFNα, TLR7/9, and CD40–CD40L interaction in Dnase 1l3−/− mice (54), our results revealed that pre-IFN granted proliferative and survival advantages to B cells stimulated via BCR triggering, even without CD40 ligation, which resulted in the activation of several B cells in SLE via extrafollicular pathways (55, 56) without the help of T cells.