In order to study the mechanisms of cytostasis in mesothelioma cells, we examined two IFN-gamma-controlled metabolic pathways known to mediate growth arrest in various cell types, measuring production of the antiproliferative compound nitric oxide (NO) and degradation of tryptophan in nine human mesothelioma cell lines (HMCLs) displaying different sensitivities to the antiproliferative effect of r-hu-IFN-gamma.