The ascites form of a diethylnitrosamine-induced hepatoma (line-1), injected intradermally into syngeneic guinea pigs, formed a local tumor which regressed. Regression was associated with development of tumor-specific cellular immunity. Tumor rejection was delayed in animals treated with complete Fruend's adjuvant (CFA) before tumor challenge. Studies on the mechanism of this delayed tumor regression showed: 1) CFA-treated animals had smaller 24-hour-skin reactions to, and prolonged rejection of, a secondtumor challenge; 2) the CFA-induced defect was corrected by systemic transfer of peritoneal exudate cells from guinea pigs immunized to the tumen 3) cutaneous inflammatory responses to turpentine and local passive transfer of tumor immunity reactions were intact in CFA-treated animalsi 4) the CFA-induced defect was systemic, i.e., it occurred even if CFA treatment was given in a way that spared nodes draining the site of tumor challengei 5) injection of CFA into animals previously immunized to tumor did not impair tumor rejection, and 6) CFA treatment abrogated induction of tumor immunity in guinea pigs challenged with a mixture of syngeneic line-10 tumor cells and BCG. CFA treatment caused systemic impairment of primary responses to tumor antigen. Effector immune mechanisms, inflammatory responses, and previously existing antigenic or tumor immunity remained intact.