Lastly, the possibility that AQP5 can function as a kinase itself should not be ignored. Another question that remains is why AQP5 is overexpressed in certain CML cells. In our FISH analysis, we found no genomic amplification of AQP5, indicating that AQP5 ICG-001 expression may be a secondary phenomenon. This is similar to our finding with AQP1 and AQP5 in lung, where no evidence for genomic amplification was detected. Currently, we are investigating the presence of AQP5 mutation with the CML samples, especially with the paired samples drawn before and after the emergence of imatinib mesylate resistance in the same CML patients. Our previous efforts to identify a promoter element responsible for the induced expression of AQP5 in several tumor cell lines suggested the existence of several potential cis-acting elements responsible for promoter activity. Moreover, methylation analysis of the AQP5 promoter region suggested that promoter demethylation may play a role in the expression of AQP5 in head and neck and lung cancer cell lines. These results, however, are still preliminary and warrant further validation. In conclusion, this is the first report, to our knowledge, to show that human AQP5 is expressed in CML cells with a potential role in cancer progression and plays a role not only in proliferation, but also in survival of CML cells. Moreover, they also provide a potential basis for designing a novel CML therapy targeting AQP5. Further expression profile studies in other hematologic malignancies such as acute leukemia and lymphoma are planned. Comprehensive functional studies to verify the novel oncogenic and anti-apoptotic properties of AQP5 in blood cancer are also warranted.. The HIV-1 envelope gene displays the largest genetic diversity in the HIV-1 genome. The evolutionary rate of env is affected by the strength of the pressure of the immune system so that both the immune pressure and the evolutionary rate are higher during the chronic, asymptomatic phase than during end-stage disease. Similarly, the immune pressure in long-term non-progressors lasts longer and is often stronger than in typical patients. Thus, HIV-1 genetic evolution in env during the chronic disease stage has been characterized by positive selection for escape mutants due to continuous immune surveillance. However, other studies have found HIV-1 evolution during chronic infection to be consistent with a neutral model of evolution, characterized by small effective population sizes strongly influenced by random genetic drift. Whether the mutation PR-171 process will be deterministic or stochastic is generally believed to be dependent on the population size. Deterministic models assume an infinite population size, which given the large amount of HIV-1 particles produced daily in an infected individual is not unreasonable. However, it has been proposed that the Ne of HIV-1 during chronic infection is several orders of magnitude lower, which would suggest that stochastic processes could influence HIV-1 evolution.