Our data indicate that normal Treg stability requires synergistical function of DGKα and ζ as DGKαζ activity serves as a signal checkpoint by braking Treg-to-exTreg/exTreg-Tfh cell conversion and by limiting numbers and functions of pathogenic IL4/13/21-expressing Tregs and exTreg/exTreg-Tfh cells to prevent IgG1-/IgE-predominant GC B-cell responses and/or autoimmunity. The gene discussed is DGKA; the disease is Autoimmunity.