To better understand the intrinsic role of glutaminolysis in lupus CD4+ T cells, we analyzed the effect of Gls1 deficiency in T cells on the autoimmune phenotypes of mice carrying the lupus-susceptibility locus Sle1b, which drives the production of autoantibodies associated with an expansion of Tfh cells and GC B cells (28, 33). The gene discussed is CD4; the disease is systemic lupus erythematosus.