Increasing evidence based on immunohistochemistry demonstrates that fibrinogen-like protein 2 (fgl2) is abundantly expressed in microcirculatory disturbances, such as in hepatic sinusoidal endothelial cells associated with human viral hepatitis [1]–[3], graft microvascular endothelial cells in allograft and xenograft rejection [4], uterus trophoblast and decidua in cytokine-induced fetal loss syndrome [5], tumor microvessel endothelium [6], and cardiac microvascular endothelial cells in type 2 diabetes or cardiac ischemia/reperfusion injury [7]–[9]. Here, FGL2 is linked to animal viral hepatitis.