In addition, blood samples were collected from hospitalized individuals undergoing coronary bypass surgery, who served as a model for major tissue surgery-induced injury which requires extensive generation of thrombin. The patient charts were reviewed and epidemiological, clinical and outcome data were collected. In order to alert a possible bias between the patient and the control groups, the age and gender of each human subject was documented. Moreover, the following patients’ parameters were documented: stage of the disease, histology, lactate dehydrogenase level, B symptoms, performance status and extranodal involvement. Patient outcomes as well as any anti neoplastic drugs administered during blood sample acquisition were also documented. Thirty two percent of Amikacin hydrate lymphoma patients were 20S-Notoginsenoside-R2 tested while not being treated with anti-neoplastic drugs, 32% were tested while receiving chemotherapy and 14% received steroid prophase while being tested. No data regarding therapy were available for 11 tested lymphoma patients. Thrombin generation was measured at regular intervals at 405 nm using an automated plate reader. Thrombin activity was calculated in each sample by comparison with a standard curve generated using known concentrations of human thrombin. FGL-2 activity is reflected by the amount of thrombin generated and expressed as a percentage relative to mean FGL-2 activity of PBMC of healthy controls. The lack of an increase in FGL-2 prothrombinase activity in situation where extensive amount of thrombin is required, such as tissue injury during coronary surgery, as has been found in this work, implied that an increase activity observed in active lymphoma patient is associated with malignant process. Moreover, the observation that a significant decrease in FGL-2 activity was measured during remission of lymphoma may suggest that monitoring of FGL-2 activity may indicate the response to treatment. Taken together, our results suggest that FGL-2 prothrombinase activity is increased in active lymphoma patients and can be used as a potential marker for the recurrence of lymphoma during remission. To date, the diagnosis of B-cell lymphoma is largely based on the pathologic workup of patients with suspicious clinical presentation. There is a deficiency of simple, non-invasive biomarkers that may assist in diagnosis and follow up of patients with lymphoma. The role of LDH as a biomarker in lymphoma has previously been explored. Published studies have demonstrated a rather low sensitivity for indolent and aggressive NHL. Recently, the sensitivity of LDH in detecting relapse of patients with DLBCL in complete remission was shown to be 69% albeit with a very low positive predictive value of 14%. Various other hematologic, morphologic and recently described molecular and genetic markers have been studied, some of which were shown to correlate with disease biology and outcome although, the sensitivity and specificity of these biomarkers for diagnosis and follow-up are not well established. In contrast to the increase in FGL-2 activity in PBMC of lymphoma patients, no increase in either mRNA or protein levels was observed. These findings may imply that the increase in FGL-2 activity measured in PBMC stems from posttranslational regulation that governs final activity. While the mechanism is yet to be determined, it is already established that a linear correlation between RNA and protein expression profile is significant in a third of human genes.