Overall, the RIP-HA model offers unique opportunities to study mechanisms of antigen-specific suppression of β cell autoimmunity, employing cotransfer of TCR-HA+ Treg cells, either with a Foxp3+ or Foxp3− phenotype, together with pathogenic T effector cells (CD4+TCR-HA+ or CD8+CL4+). The gene discussed is FOXP3; the disease is Autoimmunity.