Collectively, with our study demonstrating that CCL5 is altered in all stages of sarcoidosis it is conceivable that CCL5 via its recruitment effect on mononuclear cells, including mast cells, could be a key chemokine that is involved in the continuum of intense inflammatory injury during early stages to the more chronic inflammatory/fibrosis during late stages of pulmonary sarcoidosis. This evidence concerns the gene CCL5 and pulmonary sarcoidosis.