In an experimental model, a modulatory role for Ig/FcR signaling in Schistosoma-induced liver pathology was previously demonstrated by exacerbated hepatic granuloma formation and fibrosis detected in B cell-deficient mice, mice lacking the common FcRγ chain and mice deficient in FcεRI, the high-affinity receptor for IgE [24], [25], [64], [65]. This evidence concerns the gene FCER1G and fibrosis.