Recent work, however, shows that in certain cytokine and tissue contexts, Th2 cells can contribute to tumor rejection: they recruit and activate eosinophils (via IL-5/eotaxin) and, in some models, re-program macrophages to become tumoricidal, and activated Th2 cells themselves can acquire perforin/granzyme-dependent cytotoxicity. Here, PRF1 is linked to neoplasm.