Unfortunately, our knowledge about the function of AAM after infection with T. cruzi in vivo is rather limited but studies addressing the impact of IL-4Rα-induced Arg-1 on the permissiveness of host cells to this parasite are absolutely required because a human study points at a crucial role of the IL-4Rα for developing a cardiomyopathy, the major complication during the chronic phase of Chagas disease (23). This evidence concerns the gene IL4R and cardiomyopathy.