Although the defects are less severe compared to RANK-deficient mice, CD40−/−RANKL−/− double deficient mice displayed a greater reduction in mature mTECs and more severe autoimmune disease, implying that RANK and CD40 act cooperatively in modulation of thymic medullary microenvironment and self-tolerance [19–21]. The gene discussed is TNFRSF11A; the disease is autoimmune disease.