Experimental evidence suggests that malaria parasites do alter their investment in transmission in response to drugs. Reece, Ali, Schneider, and Babiker (2010), for example, found a decrease in conversion in human malaria parasites exposed to low doses of drugs in vitro, as our model predicts, unless they were known to be “classically” drug‐resistant parasites, which showed no change in investment (a result that highlights the multiple routes available for mitigating the effects of drugs). A similar study found no effect of drug dose on conversion rates (Peatey et al., 2009), and an in vivo rodent malaria experiment suggested that subcurative drug doses lead to increased conversion (Buckling, Taylor, Carlton, & Read, 1997). In contrast to the results of Reece et al. (2010), these latter two examples show parasite responses that appear maladaptive in the light of our model results, raising at least two further questions. First, have parasite strategies been accurately measured? Inferring conversion rates is fraught with difficulties that have only recently been resolved (Greischar et al., 2016b), and reanalysis of past data sets could reconcile the discrepancy between theoretical predictions and empirical estimates of transmission investment. Second, are parasites capable of evolving adaptive transmission strategies to the novel selection pressure of drug treatment? Addressing this question means evaluating whether the parasites in these experiments would have achieved greater fitness than ones with different responses, which necessitates tools for manipulating parasite strategies. Advances in understanding the molecular pathways associated with commitment to gametocytogenesis (e.g., Brancucci, Goldowitz, Buchholz, Werling, & Marti, 2015) may bring such tools for experimental manipulation into reach.