While the protection against autoimmune diseases in mice overexpressing BCL2 in T cells was secondary to the capacity of this anti-apoptotic molecule to control the expression of the cell cycle inhibitor p27kip1 that in turn, regulated the differentiation and activity of Tregs [12], the protection observed in young, but not old, BIM-/- [5, 10, 11] and in BCL2A1 TgT mice was associated with defects in the activation of T cells. The gene discussed is BCL2A1; the disease is autoimmune disease.