During the co-evolution of host and parasite, anti-inflammatory mechanisms have emerged, allowing the worm to suppress host immunity while ensuring host viability (thereby preserving its habitat), and enabling the host to eliminate the parasite without incurring “collateral damage.” Understanding the role of IL-22 is critical, as effective immunotherapies for schistosomiasis will necessitate a comprehensive understanding of the mechanisms underlying T cell-mediated liver immunopathology. The gene discussed is IL22; the disease is schistosomiasis.