Moreover, chronic TLR7 activation in lupus models is sufficient to cause CD11c+ B cells to differentiate and produce anti-Sm/RNP autoantibodies, whereas B-cell intrinsic TLR7 deficiency reduces the number of CD11c+ B cells and ameliorates lupus-like conditions (42). The gene discussed is ITGAX; the disease is systemic lupus erythematosus.