Our first hypothesis to help explain this observation, that bee gene families are systematically smaller than in other insects, is not supported because there is no evidence for a systematic downward bias in paralogue counts across the bee genome at the level seen for immune-gene families (Honey Bee Genome Sequencing Consortium, 2006) . Hypothesis two, that bee genes were simply missed due to sequence divergence, should apply particularly for immune genes that are short and subject only to limited sequence constraints, such as those encoding antimicrobial peptides. Indeed, few such peptides have been identified from bees (n = 6) and the means with which these few were discovered (directly at the protein level in all but one case) support the idea that sequence-level searches might have missed additional family members. Nevertheless, members of the remaining gene-poor families do not comprise especially short genes, nor genes divergent enough to be missed completely by comparisons at the level of insect orders. In fact, at least one significant bee:Drosophila:Anopheles orthologue is present in each of the remaining discussed families, indicating sufficient sequence-level conservation for identification of bee counterparts. Our third hypothesis, that bees simply have an undescribed mechanism for broadening their immune efficacy, is not testable at this point but would be very surprising given similarities in immune actors across the diverse insect orders studied to date. Two of our initial hypotheses, that bees face a less diverse set of successful parasites and pathogens, and that societal defences by bees lessen pathogen pressures, therefore seem best supported by the data in hand and can now be compared. On one level, bee pathogens are diverse, ranging from Gram-positive and Gram-negative bacteria to fungi, RNA viruses, microsporidia and amoebae (Morse & Flottum, 1997) . Bees are also parasitized by mites and other arthropods, raising risks of both pathogen infection (Kanbar & Engels, 2003; Chen et al., 2004) and lower abilities to combat disease (Gregory et al., 2005; Yang & Cox-Foster, 2005) . Still, despite having pests that range over several kingdoms, common disease agents in bees are in fact restricted to several pathogens, two of which (the bacterium Paenibacillus larvae and the fungus Ascosphaera apis) are predominant. While functional data on the specificity of responses toward these and other pathogens are not yet available, gene-expression changes after challenge do not appear to be especially precise with respect to honey bee pathogens vs. exotics (e.g. Escherichia coli) or stress generally (Fig. 3) . Thus, there is no compelling evidence at this point that the bee immune response is channelled just toward a small set of 'true' pathogens.