Under physiological conditions, homeostatic Treg numbers are maintained by low level production of IL‐2 from conventional CD4+ T cells (Tconv).12 However, this balance may become disturbed upon (repeated) exposure to foreign antigens (eg, during infections, exposure to allergens, etc. 11, 13), resulting in exaggerated CD4+ Tconv cell expansion and excess IL‐2 production, which, in turn, leads to compensatory Treg cell expansion.12 Whether and how antigen directly contributes to Treg development and expansion has been controversially discussed in the past. The gene discussed is IL2; the disease is infection.