These doses of IRF7 were chosen as they do not result in huge induction of the native IFN promoter. As shown in Figure 5A, the activation of IFN-a4P by both human and bat IRF7 was increased by co-transfection with MyD88. Co-transfection of cells with bat MyD88 and IRF7 resulted in a higher response compared to co-transfection with the corresponding human plasmids. Our results demonstrate that even with a significant difference in its MyD88 binding region, bat IRF7 is still capable of inducing IFN-a transcription via MyD88. Some differences were observed between IFN-a4 and IFN-a6 inducibility which may be due to differences in their IRF or NF-kB binding motifs. However, some genes from the B-terms of the close discovery were cell cycle regulators, suggesting that anandamide might be related to cell cycle in gastric cancer. As expected, real-time PCR and western blot assays detected that the expressions of those cell cycle regulators were significantly altered following anandamide treatment. Flow cytometry assays further confirmed that anandamide induced G2/M cell cycle arrest in gastric cancer cells through active G2/M checkpoints. This represents the first time that the cell cycle redistribution was detected in gastric cancer cells after being treated with anandamide directly and separately. Additionally, the results indicated that the B-terms could potentially function to mediate the effectors between the disease and the discovery targets. For biological investigators, keeping up-to-date with current published research is a critical component of any investigator’s job description, and nearly every published article is an opportunity to find novel links between drug and disease. Tight junctions consist of molecules such as claudin-3, claudin-5 and claudin-12, as well as other transmembrane proteins such as occludin. The disruption to the BBB surrounding tumors is thought to result from defects in these tight junctions, with abnormal expression of tight junction molecules reported to correlate with increasing malignancy. Despite extensive knowledge of the structure of the BBB, molecular mechanisms for the disruption associated with brain tumor growth remains poorly understood.