But usually, these receptors are overexpressed or constitutively active due to mutations, which lead to overactivation of downstream targets, or to misactivation of other targets. In the case of PAR1, the mechanism of action in leukemogenesis might be different. Absence of Par1 enhances leukemia development, which might indicate vice versa that wild type expression of Par is able to suppress leukemogenesis to a certain extent. Recently, it was shown that Par1 signal transduction might occur via the RhoA/ROCK1 pathway, which is also implicated to influence hematopoietic stem cells. Although it was somewhat surprising that Par1 acted as a suppressor of stem cell function in leukemia, whereas it is implicated as an oncogene in other cancer entities, several other prominent factors also display such divergent functions. One example is the polycomb complex protein EZH2 that acts as an oncogene i.e. in prostate and breast cancer, while it suppresses T-cell leukemia development in mice. In addition, Notch1 signalling is intensively studied and discussed as oncogene in different tumors and as tumor suppressor in leukemias. Therefore, it is quite possible that Par1 acts with divergent outcome in different cancers. In addition, also its close relative Par2 was already identified as tumor suppressor in a model for skin carcinogenesis, although Par2 was also mostly accepted as oncogene, which illustrates the diverse functions that can be expected in this receptor family. Finally, the fact that mice transplanted with Par1-deficient MLL-AF9 blasts benefit from the re-activation of Par1-expression might suggest that this could also help as a therapy for patients initially expressing very low or no PAR1. Rendering leukemic stem cells responsive to leukemia therapy is still a big task with the goal to be able to ultimately eradicate the disease. Further studies on the role of Par1 in different leukemias might help to understand leukemic stem cell function and to develop molecular therapies to target these cells. Lung cancer is the leading cancer-related cause of death worldwide in both men and women. In China, the mortality rate for lung cancer has increased by 465% during the last 30 years, making it the most deadly of all malignant tumors. Despite advances in treatments such as surgery, chemotherapy and radiotherapy, the clinical prognosis for patients with lung cancer remains poor, and the overall 5-year survival rate is only 10-15%. This is because at the time of diagnosis, most lung cancer patients present with an advanced stage of disease. Therefore, there is an urgent need to identify biomarkers that are useful for detection of early-stage lung cancer, and developing a prognosis for long-term survival of patients. Recently, novel technology linked to development of the human genome database has been utilized.