If the progression from replicating H. hammondi zoite to tissue cyst is as predictable in vivo as it is in vitro (which is unknown but likely given that even IFN-γ knockout mice survive infection with H. hammondi; [Dubey and Sreekumar, 2003]), and H. hammondi has non- or less-functional orthologs of genes like TgIST (Hakimi et al., 2017; Olias et al., 2016; Gay et al., 2016), this may prevent the fixation of any polymorphisms in the population that might result in the suppression of spontaneous bradyzoite conversion. This evidence concerns the gene IFNG and infection.