IL-18 has been shown to stimulate increased IFNγ production by lymphocytes isolated from COPD lung compared to smoking control tissue [5], and the cytotoxic potential of CD56+ cells increased with disease severity [6], therefore future studies should attempt to determine whether this phenotype is indeed evident within lymphoid follicles in COPD lung tissue with IL-18 as a key driver. Here, NCAM1 is linked to chronic obstructive pulmonary disease.