The fact that the use of the enzymatic inhibitor of HO-1 SnPP significantly decreased the levels of IL-10, TGFβ, and FIZZ-1 in liver, even to lower levels to control infected mice (for IL-10 and FIZZ-1) strongly suggests that HO-1 is involved in the upregulation of IL-10, promoting parasite survival, and hence liver damage that leads to the upregulation of FIZZ-1 indicating liver fibrosis. This evidence concerns the gene TGFB1 and Hepatic fibrosis.