MYD88 and infection: Curiously, although mice single deficient in TRIF or IFNAR1 (type 1 IFN receptor) were shown to be resistant to the infection with T. cruzi, Myd88−/− Ifnar1−/− double deficient mice display the same highly susceptible phenotype as Myd88−/− Trif−/− double deficient strain, pointing to a protective role for IFN-β and/or IFN-α that, however, only becomes apparent when the Myd88 pathway is absent [42].