In these lupus models and SLE patients, excessive CD11c+Tbet+ age-associated B cells were shown to induce dysregulated follicular T-helper cell differentiation, disrupting the latter to execute their potent antigen-presenting function and high-affinity selection of B cells, with subsequent paradoxical coexistence of excessive autoreactive antibodies and insufficiently affinity-matured pathogen-specific antibodies in SLE [19]. The gene discussed is TBX21; the disease is systemic lupus erythematosus.