As the infection progressed, consistent with the events occurring during other parasitic diseases induced by Schistosoma mansoni, Toxoplasma gondii and Clonorchis sinensis [39–41], CD206+ KCs (M2) predominantly had an anti-inflammatory phenotype in the strongly Th2 cytokine-rich environment [42] during the late stage after infection, and a small number of recruited MoMFs gradually repolarized toward a predominant anti-inflammatory M2 phenotype, which promoted the survival and growth of established cyst forms in the liver in the murine model. This evidence concerns the gene MRC1 and infection.