There are two major hypotheses concerning the pathogenesis of sarcoidosis. First, sarcoidosis is due to one or more environmental inhalational triggers. Second, sarcoidosis is due to an abnormal immunological host response to common antigenic triggers. Either, or both, may induce the expression of monocytic-derived cytokines and chemokines, and/or enhance Th1-type responses,6leading to the development of the prototypical microscopic finding in sarcoidosis, the epithelioid granuloma. We speculate that the postHSCT lung environment may promote nonnecrotizing epithelioid granulomatous formation caused by high levels of some of these chemokines including MCP-1, CCR1, CCR2, IL-8, and Rantes.7–8 Based on approximately 2,600 HSCTs performed over a 12-year period and 4 cases of sarcoid, we estimate the prevalence of sarcoidosis in the HSCT population to be about 150 cases per 100,000 or about 10-fold higher than that of the normal population.