Induction of delayed-type hypersensitivity challenge reactions to microbial antigens at sites of neoplasms involving the skin resulted in regression of mycosis fungoides, reticulum cell sarcoma, superficial basal cell carcinoma and adenocarcinoma of the breast. Similar reactions induced by lymphokine preparations also resulted in regression of lesions of mycosis fungoides and superficial basal cell carcinoma. The role of the large monomuclear cells in the inflammatory infiltrate of the delayed hypersensitivity reaction in eliciting the tumor regression is discussed. It is proposed that these large mononuclear cells represent the effectors in a primitive surveillance mechanism for neoplastic cells.