In our study, the simultaneous confirmation of CXCR3, T-bet, and IFN-γ expression in CD4+ cells revealed that CXCR3loT-bethi cells, rather than CXCR3hiT-betlo cells, overproduced IFN-γ and was closely involved in the pathogenesis of SLE, including treatment resistance (Figures 1, 2). This evidence concerns the gene CXCR3 and systemic lupus erythematosus.