Utilizing the same cohort of SLE patients and healthy donor IRF5-SLE homozygous risk and non-risk carriers from the GaP registry [20], we previously reported that IRF5 expression was unchanged in B cells and myeloid cells from risk and non-risk carriers, and instead, IRF5 activation or nuclear translocation was significantly elevated in the myeloid compartment of homozygous risk carriers, which mirrored that seen in SLE patients [17]. This evidence concerns the gene IRF5 and systemic lupus erythematosus.