Based on the presence of the gene encoding TLR7 in this translocated segment of the X chromosome, the possible role of TLR7 in the activation of autoreactive B cells and the development of SLE, the TLR7 gene duplication has been proposed to be the etiological basis for the Yaa-mediated enhancement of disease. This evidence concerns the gene TLR7 and systemic lupus erythematosus.