Splenocytes from the mice exhibiting tumor regression proliferated considerably in response to MUC1 peptides (Fig. 7A) and produced high levels of Ag-specific IFN-γ (Fig. 7B), indicating that malaria parasite infection augmented not only in situ immunity but also long-lasting, systemic tumor-specific immunity, contributing to the inhibition of tumorigenesis and the rejection of tumor infiltration at distant sites. Here, IFNG is linked to neoplasm.