While reproductive restraint in response to treatment can, to some extent, buffer against the effects of drugs, our models predict that treatment still leads to reductions in parasite fitness and, importantly, reductions in transmission potential. As reproductive restraint necessarily means prioritization of asexual replication and it is these parasite stages that are most responsible for the virulence (harm) of a malaria infection, there may be consequences of shifting patterns of conversion at the host (or clinical) level. Drug treatment reduces infected RBC densities, even if parasites alter their conversion rates (Figure 3), but what if parasites employ drug‐adapted strategies in an infection that remains untreated? Figure 5b shows that, in an untreated host, infections composed of parasites using a drug‐adapted strategy (coloured lines) are predicted to result in much more rapid declines in uninfected RBC densities, and greater anaemia as measured by minimum RBC counts, compared to parasites using the best strategy in the absence of drugs (black line).