TLR7 and CXorf21 (also termed TASL; TLR adapter interacting with SLC15A4 on the lysosome) also escape XCI (140, 141, 161–163), resulting in higher production of IFN-α, which is critical in driving the pathogenesis of SLE (164, 165). This evidence concerns the gene IFNA1 and systemic lupus erythematosus.