We have shown that, in principle, altered life history can protect against the effects of drugs, and while we have used a model of drug action that was parameterized for a particular drug (pyrimethamine; Huijben et al., 2013), the phenomenological description we employ should capture the effects of many different drugs. Although there will be differences among individual hosts in drug metabolism that would affect, for example, the duration of drug action, our exploration of a range of drug doses should capture much of this variation. One exception to this generality is drugs that directly target gametocytes (e.g., primaquine, White, Ashley, et al., 2014). The relative susceptibility of asexuals and gametocytes to the drug will alter the costs and benefits of producing each stage, so different drugs may be expected to have different effects on optimal patterns of transmission investment. For example, a drug with a strong gametocidal effect may generate an advantage to reproductive restraint when drugs are present but promote the production of surplus gametocytes to compensate for those killed by drugs when drugs have cleared or may promote earlier production of gametocytes to compensate for lost transmission opportunities during drug treatment. Predicting evolutionary trajectories in response to such drugs will require precise calibration of the relative susceptibility of different parasite stages.