As more facts emerge regarding the ways in which E. multilocularis-derived molecules trigger the host immune response and modulate the host-parasite interplay, it becomes possible to envisage how the parasite can survive and proliferate in its intermediate host, while in other hosts it dies out. Through effects on cells of both the innate and adaptive arms of the immune response, E. multilocularis can orchestrate a range of outcomes that are beneficial not only to the parasite, in terms of facilitating its intrahepatic proliferation and maturation, and thus life cycle over all, but also to its intermediate host, in limiting pathology. The present review deals with the role of metacestode surface molecules as well as excretory/secretory (E/S) metabolic products of the parasite in the modulation of the host responses such as to optimize its own survival.