Another model, the FRG mouse that lacks the fumarylacetoacetate hydrolase (Fah−/−) which causes liver injury, and immunocompromised (with a Rag2−/− and Il2rγ−/− background), can harbor up to 90% of human hepatocytes in the liver (94), and when crossed with NOD mice (non-obese diabetic mice that tolerate human hematopoietic cells), and transplanted with human hepatocytes and O+ human red blood cells, supports the transition of liver-stage to blood-stage malaria, after P. falciparum infection (95). Here, FAH is linked to malaria.