Recent work has focused on dormancy as another nonclassical resistance mechanism thought to be employed by malaria parasites (e.g., Codd, Teuscher, Kyle, Cheng, & Gatton, 2011; Hott et al., 2015; Paloque, Ramadani, Mercereau‐Puijalon, Augereau, & Benoit‐Vical, 2016; Teuscher et al., 2010). This delayed development confers protection against the effects of fast‐acting drugs that decay rapidly within a host, but whether such a strategy would be beneficial against drugs with longer half‐lives is unclear. Parasites can stall their intra‐erythrocytic development for many days, but only a small fraction—less than two per cent—appear to successfully recover and resume development even at low drug doses (Teuscher et al., 2010). It is not clear that such a low percentage of parasites entering dormancy can explain malaria dynamics in patients (Saralamba et al., 2011). Further, the fitness consequences of dormancy are not intuitive: surviving the effects of drugs is clearly good from the parasite's perspective, but stalling development means stalling production of transmission stages and missing out on any transmission opportunities during the dormant phase. In contrast, parasites can recover substantially more than two per cent of their numbers by modifying transmission investment under some treatment regimes. Indeed, Figure 3 suggests that parasite densities can actually increase by an order of magnitude or more within less than 4 days and this modified life history translates to fitness gains (Figure 4). It is interesting to consider how these two mechanisms of nonclassical resistance would affect host health. At least in the short term, dormancy should reduce pathology associated with parasite replication as well as immunopathology, while reduced investment in transmission is likely to do the opposite.