Cytokine-stimulated (bystander) accumulation of T cells may potentially explain allergen-independent sensitization in asthmatics, e.g., respiratory infection leading to an IL-2- or IL-15-induced proliferation of resident memory, viral antigen-non-specific, allergen-specific type 2 T cells, conditions which have been speculated to be relevant to the development of asthma [19]. The gene discussed is IL2; the disease is asthma.