Through coordinated suppression of Th1/Treg programs (via IL-2↓/TGF-β↓, T-bet↓/Foxp3↓) and potentiation of Th2/Th17 pathways (via IL-6↑/IL-17↑, GATA3↑/RORγt↑), Pvt1 overexpression establishes a pro-inflammatory milieu characteristic of active SLE. This evidence concerns the gene PVT1 and systemic lupus erythematosus.