Given the clear association of IL-18 with lymphoid aggregates, with a pattern of distribution of IL-18+ cells which closely represents that described in lymph nodes in infection (including sub-capsular like IL-18+ cells) [8], we hypothesised that the same mechanisms which relate to cellular positioning described in lymph nodes to regulate IFNγ may be important in these ectopic follicle-like structures in the lung, and therefore become increasingly dominant as COPD progresses. The gene discussed is IFNG; the disease is chronic obstructive pulmonary disease.