When designing drugs to treat infections, the invasion step is where the pathogens might be most vulnerable to pharmacological intervention. This idea is supported by studies in which parasite exposure to chemical compounds neutralizes binding to host receptors, fortifying the importance of invasion to the establishment of a clinical infection. 62, 63 Thus, many therapeutic measures against a variety of pathogens rely on this vital receptor-ligand interaction. Virus examples include the seasonal influenza vaccine, and fusion inhibitor compounds, a class of anti-HIV therapies. 64, 65 In nonvirus parasites the situation is more complicated, because the process of invasion is a complex module involving several different effectors. One possible example of a robust invasion module is in Plasmodium falciparum, the causative agent of the most deadly form of human malaria. In P. falciparum and the apicomplexan parasites, an apical complex is central to the invasion process, which includes multiple steps involving protein interactions and temporally and spatially regulated expression of proteases and polymerization machinery. 63, 66, 67 Given the importance of erythrocytes as cells where parasite replication occurs, one might expect that P. falciparum interactions with erythrocytes should be particularly critical in a robustness module for the FIG. 3 . ͑Color online͒ Robustness in gene networks of influenza A HA genes. Phenotypes are genetically robust, allowing genotypes to drift through genotypic neutral space before instant shifts in phenotype. Such a scenario is a demonstration, from the actual epidemiological literature, of how genetic robustness can facilitate evolvability in infectious disease agents. ͓From E. van Nimwegen, Science 314, 1884, 2006. Reprinted with permission from AAAS.͔ pathogen. In fact, studies show that the erythrocyteattachment process involves redundancy in ligands used for binding of the pathogen to erythrocyte receptors. 68, 62 This evolved strategy might have been selected in P. falciparum because erythrocyte receptors are highly polymorphic, perhaps among the fastest evolving genes in the human genome. 69, 70 Research shows that P. falciparum utilizes a plethora of ligands to bind erythrocyte receptors. 62, 68, 70 Interestingly, a "molecular hierarchy" may be the ideal term to describe ligand usage in P. falciparum; the pathogen's invasion module may consist of a hierarchy whereby some ligands used in attachment are preferred over others, with the switch in usage only taking place when a ligand higher up in the hierarchy is ineffective ͑Fig. 4͒. 68 This observation may be usefully couched in terms of robustness, because redundancy is a possible mechanism for constructing a robust biological system. To ensure that an essential function is carried out, a biological system can be organized to contain several alternative pathways in the event that one or more become unavailable or dysfunctional. This evolved strategy decreases the probability that an environmental perturbation disrupts performance.