As well as the relative in vitro substrate specificities of the overexpressed P450s, GSTs and CEs we describe here are warranted. We also observed several genes which exhibited strong differential expression but were among the lowest expressed of their class. It is possible that these transcripts are abundantly expressed in a limited set of tissues, which would result in an overall low measure of expression when the entire bed bug is considered. Alternatively, these gene products may exhibit high selectivity for the target insecticide molecules. Thus we cannot necessarily rule out an important role for these gene products at this time. Analysis and annotation of transcriptome sequences in the absence of a reference genome must ultimately face decision points regarding what is a separate gene, and what is polymorphism within the same gene. We were fairly conservative in treating near identical, but clearly variant sequences as a single gene. Thus, our analysis of the number of P450, GST and CE genes must be viewed as a minimum. This is especially true as our sequencing data came only from a single life stage. Ultimately, only with a full bed bug genome sequence will it be possible to distinguish between highly similar genes such as P450s, which are well-known to undergo duplications and expansions in other insect species. In conclusion, our results indicate that highly-resistant bed bug populations can have multiple genetic mechanisms conferring resistance to pyrethroid insecticides. In the case of the Richmond strain bed bugs, several forms of P450 and hydrolyzing esterases may be contributing to the bed bugs’ overall ability to reduce their pesticide load. In addition, the alpha-subunit mutation reduces the potential for any non-metabolized pyrethroid to bind at the target site. It is reasonable to suggest that the genes responsible for these resistance mechanisms have been selected for in populations that have been subjected to long-term insecticide pressure. Pancreatic cancer remains one of the most devastating cancers, and is the fourth leading cause of cancer death in western societies with a survival rate of less than 5%. Nothing apart from pancreatic resection in a proportion of patients, offers any curative potential, with chemotherapeutic agents meeting limited success. Chronic pancreatitis is a significant risk factor for the development of pancreatic cancer and both are characterised by extensive stellate cell mediated fibrosis, which in the case of pancreatic cancer facilitates cancer progression and metastasis. Recently, Olive et al demonstrated that, by targeting the stroma using inhibitors of hedgehog signalling, significantly improves the delivery of chemotherapeutic agents to the epithelial compartment of the tumor, and although the Oligomycin A effect was transient, improved overall efficacy. Further, Kraman et al demonstrated that targeting specific sub-populations of stromal cells for destruction could remove their inhibitory effect on the host’s immune response to the tumor. Observations made in recent years have demonstrated that adult stem cells have remarkable flexibility in their differentiation repertoires.