CD72 has a significant role in developing SLE-like disease in animal models; CD72 deficient mice (CD72−/−) have enhanced BCR-mediated signals that lead to more proliferative and autoreactive B cells, highly producing autoantibodies (anti-nuclear and anti–ds DNA) and spontaneously develop lupus-like disease features when they age (Li et al., 2008). This evidence concerns the gene CD72 and systemic lupus erythematosus.